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Volume 17,Issue 5,2010 Table of Contents
2010, 17(5):487-491.
DOI: 10.3872/j.issn.1007-385X.2010.5.001
Abstract:
In addition to the cancer cells, there are many other cells in the tumor microenvironment, such as the stromal cells, endothelial cells, CD4+ and CD8+ lymphocytes, NK cells, macrophages and neutrophils, etc. Recent studies have found that tumor-associated neutrophils (TANs) play important roles in the development and progression of tumors. TANs can promote tumor development and metastasis through various mechanisms, such as TANs promoting tumor proliferation and metastasis by secreting elastase, promoting tumor angiogenesis by secreting matrix metalloproteinase, and highly activated TANs exerting anti-tumor activity by killing tumor cells. Further study on TANs casts new lights on immunotherapy of tumors; and using TANs and molecules secreted by TANs as targets may become an important strategy for inhibiting the development and progression of tumors.
In addition to the cancer cells, there are many other cells in the tumor microenvironment, such as the stromal cells, endothelial cells, CD4+ and CD8+ lymphocytes, NK cells, macrophages and neutrophils, etc. Recent studies have found that tumor-associated neutrophils (TANs) play important roles in the development and progression of tumors. TANs can promote tumor development and metastasis through various mechanisms, such as TANs promoting tumor proliferation and metastasis by secreting elastase, promoting tumor angiogenesis by secreting matrix metalloproteinase, and highly activated TANs exerting anti-tumor activity by killing tumor cells. Further study on TANs casts new lights on immunotherapy of tumors; and using TANs and molecules secreted by TANs as targets may become an important strategy for inhibiting the development and progression of tumors.
WANG Gang
,
DONG Xiao-yan
,
TIAN Wen-hong
,
YUCHI Jie
,
HU Jian-yang
,
FU Xin-yang
,
LIU Yun-fan
,
TAN Wen-jie
,
WU Xiao-bing
2010, 17(5):492-498.
DOI: 10.3872/j.issn.1007-385X.2010.5.002
Abstract:
Objective:o investigate the regulatory effect of liver-specific microRNA-122(miR-122) on the expression of exogenous genes and its role in decreasing the liver toxicity of herpes simplex virus type 1-thymidine kinase/gancyclovir (TK/GCV) therapy system. Methods: MiR-122-regulated pEGFP-122T, pLuc-122T or pTK-122T plasmids were constructed by inserting miR-122 targeting sequence into the 3′-untranslated region (3′-UTR) of the corresponding genes, and the plasmids were then transfected into miR-122-positive Huh7 and miR-122-negative HeLa cells, then the expression of reporter genes and the hepatotoxicity of TK/GCV system were observed. After hydrodynamic delivery of relevant plasmids into mouse liver, the expressions of EGFP and Luc were analyzed by fluorescence microscopy and in vivo bioluminescent imaging; and the hepatotoxicity of TK/GCV system on mice was evaluated by serum ALT, weight, survival and hepatic histology. Results: In Huh7 cells, the EGFP expression and Luc activity were inhibited by miR-122 targeting sequence insertion, and pTK-122T-transfected Huh7 cells showed resistance to cytotoxicity of TK/GCV system; whereas in HeLa cells, the expression of reporter genes and the cytotoxicity of TK/GCV system were not influenced. In vivo results showed that hepatocytes in pEGFP-122T-treated mice did not express EGFP, but 30% hepatocytes in pEGFP-treated mice expressed high level of EGFP; the Luc activity was significantly down-regulated in pLuc-122T-treated mice compared to pLuc-treated mice. Hydrodynamic injection of pTK-122T caused no increase of serum ALT level or decrease of body weight, liver toxicity of GCV treatment, while significant increase of serum ALT level, decrease of body weight and severe liver damages were found in the pTK-treated mice. Conclusion: MiR-122 targeting sequence insertion can inhibit the expression of exogenous genes in the liver, and can effectively decrease the hepatotoxicity of TK/GCV system.
Objective:o investigate the regulatory effect of liver-specific microRNA-122(miR-122) on the expression of exogenous genes and its role in decreasing the liver toxicity of herpes simplex virus type 1-thymidine kinase/gancyclovir (TK/GCV) therapy system. Methods: MiR-122-regulated pEGFP-122T, pLuc-122T or pTK-122T plasmids were constructed by inserting miR-122 targeting sequence into the 3′-untranslated region (3′-UTR) of the corresponding genes, and the plasmids were then transfected into miR-122-positive Huh7 and miR-122-negative HeLa cells, then the expression of reporter genes and the hepatotoxicity of TK/GCV system were observed. After hydrodynamic delivery of relevant plasmids into mouse liver, the expressions of EGFP and Luc were analyzed by fluorescence microscopy and in vivo bioluminescent imaging; and the hepatotoxicity of TK/GCV system on mice was evaluated by serum ALT, weight, survival and hepatic histology. Results: In Huh7 cells, the EGFP expression and Luc activity were inhibited by miR-122 targeting sequence insertion, and pTK-122T-transfected Huh7 cells showed resistance to cytotoxicity of TK/GCV system; whereas in HeLa cells, the expression of reporter genes and the cytotoxicity of TK/GCV system were not influenced. In vivo results showed that hepatocytes in pEGFP-122T-treated mice did not express EGFP, but 30% hepatocytes in pEGFP-treated mice expressed high level of EGFP; the Luc activity was significantly down-regulated in pLuc-122T-treated mice compared to pLuc-treated mice. Hydrodynamic injection of pTK-122T caused no increase of serum ALT level or decrease of body weight, liver toxicity of GCV treatment, while significant increase of serum ALT level, decrease of body weight and severe liver damages were found in the pTK-treated mice. Conclusion: MiR-122 targeting sequence insertion can inhibit the expression of exogenous genes in the liver, and can effectively decrease the hepatotoxicity of TK/GCV system.
2010, 17(5):499-504.
DOI: 10.3872/j.issn.1007-385X.2010.5.003
Abstract:
Objective:To investigate folic acid receptor-mediated targeted gene delivery of chitosan-pGPU6/GFP/Neo nanoparticles to tumor cells expressing different degrees of folic acid receptors. Methods: Folate-chitosan-pGPU6/GFP/Neo nanoparticles (FA-CS-DNAnano) and chitosan-pGPU6/GFP/Neo nanoparticles (CS-DNAnano) were prepared and identified by infrared spectrometer, and their morphology characteristics and diameters were observed under transmission electron microscope. Human ovarian cancer cell line SKOV3, breast cancer cell line MCF-7, and cervical cancer line HeLa were transfected with the prepared nanoparticles; the transfection efficiency was evaluated by flow cytometry; and cytotoxicities of the nanoparticles were detected by MTT method. Results: FA-CS-DNAnano and CS-DNAnano were successfully prepared. The particles had a smooth surface and a uniform structure, with the diameters being (78.1±0.3) nm and (1384±0.7) nm. Transfection efficiency of FA-CS-DNAnano was significantly higher than that of CS-DNAnano in SKOV3 and MCF-7 cells (\[24.3±0.7\]% vs \[0.7±0.1\]%, \[16.8±1.2\]% vs \[0.3±0.1\]%; all P<0.01), but not in HeLa cells (P>0.05). The cell vitalities of MCF-7, SKOV3 and HeLa cells were (87.9±2.4)%, (91.4±10)%, (97.4±1.1)% before transfection, and were (63.0±2.5)%, (90.6±1.3)%, and (99.3±1.6)% after transfection with FA-CS-DNAnano. Conclusion: Chitosan modified with folic acid is an efficient target gene carrier for folic acid receptor highly positive SKOV3 and MCF-7 tumor cells.
Objective:To investigate folic acid receptor-mediated targeted gene delivery of chitosan-pGPU6/GFP/Neo nanoparticles to tumor cells expressing different degrees of folic acid receptors. Methods: Folate-chitosan-pGPU6/GFP/Neo nanoparticles (FA-CS-DNAnano) and chitosan-pGPU6/GFP/Neo nanoparticles (CS-DNAnano) were prepared and identified by infrared spectrometer, and their morphology characteristics and diameters were observed under transmission electron microscope. Human ovarian cancer cell line SKOV3, breast cancer cell line MCF-7, and cervical cancer line HeLa were transfected with the prepared nanoparticles; the transfection efficiency was evaluated by flow cytometry; and cytotoxicities of the nanoparticles were detected by MTT method. Results: FA-CS-DNAnano and CS-DNAnano were successfully prepared. The particles had a smooth surface and a uniform structure, with the diameters being (78.1±0.3) nm and (1384±0.7) nm. Transfection efficiency of FA-CS-DNAnano was significantly higher than that of CS-DNAnano in SKOV3 and MCF-7 cells (\[24.3±0.7\]% vs \[0.7±0.1\]%, \[16.8±1.2\]% vs \[0.3±0.1\]%; all P<0.01), but not in HeLa cells (P>0.05). The cell vitalities of MCF-7, SKOV3 and HeLa cells were (87.9±2.4)%, (91.4±10)%, (97.4±1.1)% before transfection, and were (63.0±2.5)%, (90.6±1.3)%, and (99.3±1.6)% after transfection with FA-CS-DNAnano. Conclusion: Chitosan modified with folic acid is an efficient target gene carrier for folic acid receptor highly positive SKOV3 and MCF-7 tumor cells.
2010, 17(5):505-509.
DOI: 10.3872/j.issn.1007-385X.2010.5.004
Abstract:
Objective:To investigate the inhibitory effect of attenuated salmonella typhimurium vaccine, which expressing xenogeneic chicken EGFR and IgG γFc, on the growth of Lewis lung cancer (expressed high level of EGFR)-implanted tumors in mice. Methods: pVAX1/ cEGFR-γFc plasmid was transformed into attenuated salmonella typhimurium strain SL7207, and the resultant SL7207/pVAX1-cEGFR-γFc bacteria were used to infect murine peripheral macrophage in vitro. Then expression of cEGFR-γFc fusion protein was detected by immunofluorescent assay. Mice were immunized with SL7207/pVAX1-cEGFR-γFc for 3 times, and then inoculated with Lewis cells. Expression of cEGFR-γFc fusion protein in mice tissue was detected by Western blotting analysis, and serum anti-EGFR level was determined by ELISA method. The weight of implanted Lewis tumor was measured after 14 d to investigate the anti-tumor effect of SL7207/pVAX1-cEGFR-γFc vaccine, and the survival time of tumor-bearing mice was also examined. Results: The attenuated salmonella typhimurium DNA vaccine SL7207/pVAX1- cEGFR-γFc was successfully constructed. The cEGFR-γFc fusion protein could be expressed in mouse cells after SL7207/pVAX1-cEGFR-γFc infection in vitro and in vivo. The mice immunized with SL7207/pVAX1-cEGFR-γFc could produce high level of anti-EGFR antibody. The tumor growth was obviously inhibited and the survival time of tumor-bearing mice was also increased in the SL7207/pVAX1-cEGFR-γFc vaccine group. Conclusion: The DNA vaccine expressing xenogeneic EGFR can effectively inhibit the growth of EGFR-positive tumors, which is a new EGFR-targeting therapy strategy.
Objective:To investigate the inhibitory effect of attenuated salmonella typhimurium vaccine, which expressing xenogeneic chicken EGFR and IgG γFc, on the growth of Lewis lung cancer (expressed high level of EGFR)-implanted tumors in mice. Methods: pVAX1/ cEGFR-γFc plasmid was transformed into attenuated salmonella typhimurium strain SL7207, and the resultant SL7207/pVAX1-cEGFR-γFc bacteria were used to infect murine peripheral macrophage in vitro. Then expression of cEGFR-γFc fusion protein was detected by immunofluorescent assay. Mice were immunized with SL7207/pVAX1-cEGFR-γFc for 3 times, and then inoculated with Lewis cells. Expression of cEGFR-γFc fusion protein in mice tissue was detected by Western blotting analysis, and serum anti-EGFR level was determined by ELISA method. The weight of implanted Lewis tumor was measured after 14 d to investigate the anti-tumor effect of SL7207/pVAX1-cEGFR-γFc vaccine, and the survival time of tumor-bearing mice was also examined. Results: The attenuated salmonella typhimurium DNA vaccine SL7207/pVAX1- cEGFR-γFc was successfully constructed. The cEGFR-γFc fusion protein could be expressed in mouse cells after SL7207/pVAX1-cEGFR-γFc infection in vitro and in vivo. The mice immunized with SL7207/pVAX1-cEGFR-γFc could produce high level of anti-EGFR antibody. The tumor growth was obviously inhibited and the survival time of tumor-bearing mice was also increased in the SL7207/pVAX1-cEGFR-γFc vaccine group. Conclusion: The DNA vaccine expressing xenogeneic EGFR can effectively inhibit the growth of EGFR-positive tumors, which is a new EGFR-targeting therapy strategy.
GONG Xin-jiang
,
WANG Dong-hai
,
ZHAO E
,
ZHENG Qing-mei
,
WANG Ke-bo
,
GAO Yong-hong
,
FAN Chuan-wen
,
ZHU Yi-dong
,
YANG Qing-min
,
WANG Jing-yi
2010, 17(5):510-513.
DOI: 10.3872/j.issn.1007-385X.2010.5.005
Abstract:
Objective:To determine the inhibitory effect of anti-gastrin vaccine mG17-CRM197 (G17) alone or in combination with 5-FU on the growth of mouse transplanted C38 colon tumors. Methods: Gastrin receptor (CCKBR) expression in C38 cells was detected by Western blotting analysis, and the influence of G17 on proliferation of C38 cells was examined by sulforhodamine B（SRB）assay. C57BL/6 mice were randomly divided into 5 groups: PBS, CRM197, G17, 5-FU and G17/5-FU. The anti-G17 levels in mouse serum were measured by ELISA assay after immunization. After immunization, mice were subcutaneously injected with C38 cells, and then treated with 5-FU (20 mg/kg, q2d×5) in 5-FU and mG17/5-FU groups, or treated with 0.9% sodium chloride in the other groups. The influences of different therapies on the growth of C38-implanted tumors were evaluated by tumor growth-curves and tumor weights. Results: Mouse colon cancer C38 cells expressed CCKBR; mG17-NH2 dose-dependently increased the expression of CCKBR. Exogenous mG17-NH2 increased the proliferation of C38 cells, with the proliferation rate being 115.7%-133.5%. Mouse serum anti-G17 antibody was increased after immunization with G17 vaccine for 3 times. The tumor growth and tumor weights were significantly inhibited in G17, 5-FU and mG17/5-FU groups, with inhibitory rates being 58.0%, 60.5% and 80.7%, respectively (P<0.05), and tumor weight in mG17/5-FU group was less than those in the G17 and 5-FU groups. Conclusion：G17-CRM197 vaccine can inhibit the growth of mouse transplanted C38 colon tumors, and the inhibitory effect is enhanced when it is combined with 5-FU.
Objective:To determine the inhibitory effect of anti-gastrin vaccine mG17-CRM197 (G17) alone or in combination with 5-FU on the growth of mouse transplanted C38 colon tumors. Methods: Gastrin receptor (CCKBR) expression in C38 cells was detected by Western blotting analysis, and the influence of G17 on proliferation of C38 cells was examined by sulforhodamine B（SRB）assay. C57BL/6 mice were randomly divided into 5 groups: PBS, CRM197, G17, 5-FU and G17/5-FU. The anti-G17 levels in mouse serum were measured by ELISA assay after immunization. After immunization, mice were subcutaneously injected with C38 cells, and then treated with 5-FU (20 mg/kg, q2d×5) in 5-FU and mG17/5-FU groups, or treated with 0.9% sodium chloride in the other groups. The influences of different therapies on the growth of C38-implanted tumors were evaluated by tumor growth-curves and tumor weights. Results: Mouse colon cancer C38 cells expressed CCKBR; mG17-NH2 dose-dependently increased the expression of CCKBR. Exogenous mG17-NH2 increased the proliferation of C38 cells, with the proliferation rate being 115.7%-133.5%. Mouse serum anti-G17 antibody was increased after immunization with G17 vaccine for 3 times. The tumor growth and tumor weights were significantly inhibited in G17, 5-FU and mG17/5-FU groups, with inhibitory rates being 58.0%, 60.5% and 80.7%, respectively (P<0.05), and tumor weight in mG17/5-FU group was less than those in the G17 and 5-FU groups. Conclusion：G17-CRM197 vaccine can inhibit the growth of mouse transplanted C38 colon tumors, and the inhibitory effect is enhanced when it is combined with 5-FU.
2010, 17(5):514-520.
DOI: 10.3872/j.issn.1007-385X.2010.5.006
Abstract:
Objective:To explore the in vitro and in vivo effects of CD40L-expressing murine colon cancer colon26 vaccine on activities of dendritic cells (DCs). Methods: The CD40L gene was transfected into colon26 cells using lipofactamine method, and the stable colon26/CD40L transfectants were obtained. Colon26/CD40L cells were co-cultured with DCs, and the phenotype of DCs was examined by flow cytometry; the expressions of cytokine genes such as IL-12, IL-23, IL-18 and IFN-γ were examined by RT-PCR; and the IL-12, IL-23 and IFN-γ levels in co-cultured supernatants were measured by ELISA. Tumor-bearing BALB/c mouse model was prepared by subcutaneous injection of colon26 cells, and treated with DCs impulsed with colon26/CD40L vaccine. IL-12, IL-23, IFN-γ, IL-10 and TGF-β levels in mouse peripheral blood were detected by ELISA; and the histopathological changes of the liver, spleen and tumor tissues were observed by H-E staining. Results: Colon26 cells stably expressing CD40L (colon26/CD40L vaccine) were successfully obtained. DCs, when co-cultured with colon26/CD40L vaccine, had up-regulated expressions of co-stimulatory molecules, including CD80, CD86, MHCⅠ and MHCⅡ (P<0.01). The expressions of IL-12, IL-23, IL-18 and IFN-γ mRNA genes were only detected in DC-colon26/CD40L system, not in other co-cultured systems. And the DC-colon26/CD40L co-cultured system showed higher IL-12, IL-23 and IFN-γ levels (P<0.01). Compared with mice treated with colon26/CD40L or DCs, mice treated with DCs-colon26/CD40L had smaller tumor volumes and lower weights (P<0.05), increased IL-12, IL-23, and IFN-γ levels in the peripheral blood (P<0.01), decreased IL-10 and TGF-β levels (P<001), and better histopathological changes of tumor tissues. Conclusion: CD40L-expressing colon cancer cells can promote the maturation, induce the cytokine secretion, and enhance the activities of DCs in vitro and in vivo.
Objective:To explore the in vitro and in vivo effects of CD40L-expressing murine colon cancer colon26 vaccine on activities of dendritic cells (DCs). Methods: The CD40L gene was transfected into colon26 cells using lipofactamine method, and the stable colon26/CD40L transfectants were obtained. Colon26/CD40L cells were co-cultured with DCs, and the phenotype of DCs was examined by flow cytometry; the expressions of cytokine genes such as IL-12, IL-23, IL-18 and IFN-γ were examined by RT-PCR; and the IL-12, IL-23 and IFN-γ levels in co-cultured supernatants were measured by ELISA. Tumor-bearing BALB/c mouse model was prepared by subcutaneous injection of colon26 cells, and treated with DCs impulsed with colon26/CD40L vaccine. IL-12, IL-23, IFN-γ, IL-10 and TGF-β levels in mouse peripheral blood were detected by ELISA; and the histopathological changes of the liver, spleen and tumor tissues were observed by H-E staining. Results: Colon26 cells stably expressing CD40L (colon26/CD40L vaccine) were successfully obtained. DCs, when co-cultured with colon26/CD40L vaccine, had up-regulated expressions of co-stimulatory molecules, including CD80, CD86, MHCⅠ and MHCⅡ (P<0.01). The expressions of IL-12, IL-23, IL-18 and IFN-γ mRNA genes were only detected in DC-colon26/CD40L system, not in other co-cultured systems. And the DC-colon26/CD40L co-cultured system showed higher IL-12, IL-23 and IFN-γ levels (P<0.01). Compared with mice treated with colon26/CD40L or DCs, mice treated with DCs-colon26/CD40L had smaller tumor volumes and lower weights (P<0.05), increased IL-12, IL-23, and IFN-γ levels in the peripheral blood (P<0.01), decreased IL-10 and TGF-β levels (P<001), and better histopathological changes of tumor tissues. Conclusion: CD40L-expressing colon cancer cells can promote the maturation, induce the cytokine secretion, and enhance the activities of DCs in vitro and in vivo.
WANG Hong
,
LIU Guang-xian
,
ZHUO Hai-long
,
BAI Wen-lin
,
WU Yu
,
ZHOU Lin
,
LOU Min
,
ZENG Zhen
,
CHANG Xiu-juan
,
XU Jian-ming
2010, 17(5):521-524.
DOI: 10.3872/j.issn.1007-385X.2010.5.007
Abstract:
Objective:To observe the efficacy of endothelial progenitor cells carrying hIFN-γ (EPCs-hIFN-γ) in cancer maintenance therapy after chemotherapy. Methods: MTT was used to examine the inhibitory effects of hIFN-γ and/or C225 against colorectal cancer LoVo cells after treatment with CPT-11. The in vivo inhibitory effects of EPCs-hIFN-γ and/or C225 on LoVo tumors and their effects on survival of LoVo tumor-bearing nude mice were investigated after mice had been treated with CPT-11. Results: In vitro, hIFN-γ and/or C225 further inhibited the growth of cancer cells after CPT-11 treatment. In vivo, after 50 mg/kg CPT-11 treatment, EPCs-hIFN-γ，C225 and EPCs-hIFN-γ+C225 inhibited the growth of tumors in LoVo tumor-bearing nude mice (mean tumor volumes: \[2024.28±1048.40\] mm3 vs \[764.94±720.14\], \[233.85±186.97\], \[186.95±133.43\], \[163.9±173.39\] mm3; P＜0.05). EPCs-hIFN-γ, C225 and EPCs-hIFN-γ+C225 treatment also increased the survival of tumor-bearing mice (median survival: 34.2 d vs 39.4, 445, 48.5, 51.3 d; P<0.05 or P<0.01). Conclusion: EPC-hIFN-γ can inhibit the tumor growth and prolong the survival of tumor-bearing mice in cancer maintenance therapy after chemotherapy.
Objective:To observe the efficacy of endothelial progenitor cells carrying hIFN-γ (EPCs-hIFN-γ) in cancer maintenance therapy after chemotherapy. Methods: MTT was used to examine the inhibitory effects of hIFN-γ and/or C225 against colorectal cancer LoVo cells after treatment with CPT-11. The in vivo inhibitory effects of EPCs-hIFN-γ and/or C225 on LoVo tumors and their effects on survival of LoVo tumor-bearing nude mice were investigated after mice had been treated with CPT-11. Results: In vitro, hIFN-γ and/or C225 further inhibited the growth of cancer cells after CPT-11 treatment. In vivo, after 50 mg/kg CPT-11 treatment, EPCs-hIFN-γ，C225 and EPCs-hIFN-γ+C225 inhibited the growth of tumors in LoVo tumor-bearing nude mice (mean tumor volumes: \[2024.28±1048.40\] mm3 vs \[764.94±720.14\], \[233.85±186.97\], \[186.95±133.43\], \[163.9±173.39\] mm3; P＜0.05). EPCs-hIFN-γ, C225 and EPCs-hIFN-γ+C225 treatment also increased the survival of tumor-bearing mice (median survival: 34.2 d vs 39.4, 445, 48.5, 51.3 d; P<0.05 or P<0.01). Conclusion: EPC-hIFN-γ can inhibit the tumor growth and prolong the survival of tumor-bearing mice in cancer maintenance therapy after chemotherapy.
2010, 17(5):525-530.
DOI: 10.3872/j.issn.1007-385X.2010.5.008
Abstract:
Objective:To construct a cathepsin L (CTSL)-siRNA eukaryotic expression plasmid and investigate its influence on the invasion and migration of ovarian cancer cells. Methods: Four pairs of small interfering RNA sequences targeting CTSL were designed and synthesized, and were transfected into ovarian cancer A2780 cells. CTSL expressions were analyzed by RT-PCR in different CTSL-siRNA transfected-A2780 cells, and the siRNA pair with the best interfering effect was chosen; the corresponding CTSL-shRNA was synthesized and inserted into psilence4.1-CMV-neo plasmid to construct psilence4.1-CTSL plasmid. Psilence4.1-CTSL was then transfected into A2780 cells and the stable transfectant A2780-CTSL was obtained. The interfering effect of psilence4.1-CTSL was detected by RT-PCR and Western blotting analysis; the proliferation of A2780 cells was examined by MTT and colony formation assay; the cell cycle of A2780 cells was measured by flow cytometry; and the invasion and migration of A2780 cells were detected by Transwell chamber assay. Results: The siRNA-CTSL-1202 sequence with the best interfering effect was selected and the corresponding CTSL-shRNA expression plasmid psilence4.1-CTSL was successfully constructed. CTSL expression in psilence4.1-CTSL-stably transfected A2780 cells was significantly decreased. The invasion and migration of A2780 cells were inhibited by CTSL silence, while their proliferation, cell cycle and adhesion were not significantly influenced. Conclusion: The siRNA eukaryotic expression plasmid targeting CTSL gene is successfully constructed, and interfering CTSL expression can suppress invasion and migration of ovarian cancer cells.
Objective:To construct a cathepsin L (CTSL)-siRNA eukaryotic expression plasmid and investigate its influence on the invasion and migration of ovarian cancer cells. Methods: Four pairs of small interfering RNA sequences targeting CTSL were designed and synthesized, and were transfected into ovarian cancer A2780 cells. CTSL expressions were analyzed by RT-PCR in different CTSL-siRNA transfected-A2780 cells, and the siRNA pair with the best interfering effect was chosen; the corresponding CTSL-shRNA was synthesized and inserted into psilence4.1-CMV-neo plasmid to construct psilence4.1-CTSL plasmid. Psilence4.1-CTSL was then transfected into A2780 cells and the stable transfectant A2780-CTSL was obtained. The interfering effect of psilence4.1-CTSL was detected by RT-PCR and Western blotting analysis; the proliferation of A2780 cells was examined by MTT and colony formation assay; the cell cycle of A2780 cells was measured by flow cytometry; and the invasion and migration of A2780 cells were detected by Transwell chamber assay. Results: The siRNA-CTSL-1202 sequence with the best interfering effect was selected and the corresponding CTSL-shRNA expression plasmid psilence4.1-CTSL was successfully constructed. CTSL expression in psilence4.1-CTSL-stably transfected A2780 cells was significantly decreased. The invasion and migration of A2780 cells were inhibited by CTSL silence, while their proliferation, cell cycle and adhesion were not significantly influenced. Conclusion: The siRNA eukaryotic expression plasmid targeting CTSL gene is successfully constructed, and interfering CTSL expression can suppress invasion and migration of ovarian cancer cells.
HAN Gou-sheng
,
LIU Jian-min
,
YUE Zhi-jian
,
HU Xiao-wu
,
SHENG Wei-hua
,
MIAO Jing-cheng
,
WANG Xiao-hua
,
YANG Ji-cheng
2010, 17(5):531-535.
DOI: 10.3872/j.issn.1007-385X.2010.5.009
Abstract:
Objective: To investigate the inhibitory effect of adenovirus-mediated IL-24 (Ad-IL-24) on human glioma U87MG cells and to explore the underlying molecule mechanism. Methods: U87MG cells were infected with Ad-IL-24 constructed in our department, and IL-24 gene expression in U87MG cells was detected by RT-PCR. The growth and apoptosis of U87MG cells were examined by MTT and flow cytometry; the morphological change of U87MG cells was observed by laser scanning confocal microscopy; the Bax and Bcl-2 mRNA expressions were analyzed by RT-PCR; and the activation of caspase-3 was examined by Western blotting analysis. Results: The IL-24 gene was expressed in Ad-IL-24-infected U87MG cells. Ad-IL-24-infection inhibited the growth and induced apoptosis of U87MG cells, which showed typical morphological changes of apoptotic nuclei. Moreover, Ad-IL-24 increased Bax and decreased Bcl-2 mRNA expression, and induced caspase-3 activation in U87MG cells. Conclusion: Ad-IL-24 can induce apoptosis of U87MG cells, probably through up-regulating Bax expression, down-regulating Bcl-2 expression, and inducing caspase-3 activation.
Objective: To investigate the inhibitory effect of adenovirus-mediated IL-24 (Ad-IL-24) on human glioma U87MG cells and to explore the underlying molecule mechanism. Methods: U87MG cells were infected with Ad-IL-24 constructed in our department, and IL-24 gene expression in U87MG cells was detected by RT-PCR. The growth and apoptosis of U87MG cells were examined by MTT and flow cytometry; the morphological change of U87MG cells was observed by laser scanning confocal microscopy; the Bax and Bcl-2 mRNA expressions were analyzed by RT-PCR; and the activation of caspase-3 was examined by Western blotting analysis. Results: The IL-24 gene was expressed in Ad-IL-24-infected U87MG cells. Ad-IL-24-infection inhibited the growth and induced apoptosis of U87MG cells, which showed typical morphological changes of apoptotic nuclei. Moreover, Ad-IL-24 increased Bax and decreased Bcl-2 mRNA expression, and induced caspase-3 activation in U87MG cells. Conclusion: Ad-IL-24 can induce apoptosis of U87MG cells, probably through up-regulating Bax expression, down-regulating Bcl-2 expression, and inducing caspase-3 activation.
2010, 17(5):536-540.
DOI: 10.3872/j.issn.1007-385X.2010.5.010
Abstract:
Objective:To study the role of a demethylating agent, 5-Aza-2′-deoxycytidine (5-Aza-CdR),in inducing NY-ESO-1 antigen expression in tumor cells. Methods: Human gastric cancer cell line SGC-7901, hepatoma cell lines H2P and MHCC97-H, colon cancer cell lines HT-29 and LoVo, and glioma cell line U251 were used in the present study. NY-ESO-1 mRNA and protein expressions were detected by RT-PCR and immunocytochemistry in the above cell lines before and after 5-Aza-CdR treatment. Results: NY-ESO-1 antigen was positive only in gastric cancer cell line SGC-7901 as detected by RT-PCR and immunocytochemistry. The morphology and growth of hepatoma cell H2P, colon cancer cell LoVo and glioma cell U251 were not obviously affected after 5-Aza-CdR treatment (1 μmol/L, 5 μmol/L and 10 μmol/L ) for 6 days; however, 5-Aza-CdR induced NY-ESO-1 mRNA and protein expressions in these cell lines in a dose-dependent manner. Conclusion: 5-Aza-CdR can induce the expression of NY-ESO-1 antigen in hepatoma, colon cancer and glioma cells, which casts new lights on tumor immunotherapy.
Objective:To study the role of a demethylating agent, 5-Aza-2′-deoxycytidine (5-Aza-CdR),in inducing NY-ESO-1 antigen expression in tumor cells. Methods: Human gastric cancer cell line SGC-7901, hepatoma cell lines H2P and MHCC97-H, colon cancer cell lines HT-29 and LoVo, and glioma cell line U251 were used in the present study. NY-ESO-1 mRNA and protein expressions were detected by RT-PCR and immunocytochemistry in the above cell lines before and after 5-Aza-CdR treatment. Results: NY-ESO-1 antigen was positive only in gastric cancer cell line SGC-7901 as detected by RT-PCR and immunocytochemistry. The morphology and growth of hepatoma cell H2P, colon cancer cell LoVo and glioma cell U251 were not obviously affected after 5-Aza-CdR treatment (1 μmol/L, 5 μmol/L and 10 μmol/L ) for 6 days; however, 5-Aza-CdR induced NY-ESO-1 mRNA and protein expressions in these cell lines in a dose-dependent manner. Conclusion: 5-Aza-CdR can induce the expression of NY-ESO-1 antigen in hepatoma, colon cancer and glioma cells, which casts new lights on tumor immunotherapy.
2010, 17(5):541-544.
DOI: 10.3872/j.issn.1007-385X.2010.5.011
Abstract:
Objective:To study the genetic damage of preliminarily diagnosed leukemia patients by micronucleus analysis technology. Methods: Peripheral blood of 54 preliminarily diagnosed leukemia patients (11 CML patients, 7 AML-M1 patients, 6 AML-M2 patients, 4 AML-M3 patients, 2 AML-M4 patients, 4 AML-M5 patients, 2 AML-M6 patients, and 18 ALL patients) and 30 healthy volunteers were collected and examined by cell cycle block test. The genetic damages of patients were assessed by micronucleus rate (MNR), micronucleus cell rate (MCR), nuclear bud (Bud) frequency, nucleoplasmic bridge (NPB) frequency, nuclear division index (NDI), and apoptotic cell (AC) rate combined with chromosome metaphase, gene fusion and gene rearrangement analysis. Results: The chromosome damages in 54 leukemia patients were significantly different from those in the 30 healthy volunteers, with MNR being (17.368±1.305)‰ vs (7368±0.844)‰, MCR being (15.418±1.212)‰ vs (5.887±1.101)‰, Bud frequency being (8.142±0132)% vs (0.404±0.404)%, NPB frequency being (5.724±0.874)% vs (0.034±0.034)%, NDI being (1.722±0.062)% vs (2.282±0.324)%, AC rate being (2.167±0.333)% vs (0.167±0.667)%, abnormal chromosome detection rate being 24.00%, gene fusion or gene rearrangement positive rate being 18.00% (P<0.05 or P<001). Conclusion: Leukemia patients show different degrees of inheritance chromosome damages in the initial stage, indicating that the inheritance damage caused by chromosomal instability is related to leukemia pathogenesis.
Objective:To study the genetic damage of preliminarily diagnosed leukemia patients by micronucleus analysis technology. Methods: Peripheral blood of 54 preliminarily diagnosed leukemia patients (11 CML patients, 7 AML-M1 patients, 6 AML-M2 patients, 4 AML-M3 patients, 2 AML-M4 patients, 4 AML-M5 patients, 2 AML-M6 patients, and 18 ALL patients) and 30 healthy volunteers were collected and examined by cell cycle block test. The genetic damages of patients were assessed by micronucleus rate (MNR), micronucleus cell rate (MCR), nuclear bud (Bud) frequency, nucleoplasmic bridge (NPB) frequency, nuclear division index (NDI), and apoptotic cell (AC) rate combined with chromosome metaphase, gene fusion and gene rearrangement analysis. Results: The chromosome damages in 54 leukemia patients were significantly different from those in the 30 healthy volunteers, with MNR being (17.368±1.305)‰ vs (7368±0.844)‰, MCR being (15.418±1.212)‰ vs (5.887±1.101)‰, Bud frequency being (8.142±0132)% vs (0.404±0.404)%, NPB frequency being (5.724±0.874)% vs (0.034±0.034)%, NDI being (1.722±0.062)% vs (2.282±0.324)%, AC rate being (2.167±0.333)% vs (0.167±0.667)%, abnormal chromosome detection rate being 24.00%, gene fusion or gene rearrangement positive rate being 18.00% (P<0.05 or P<001). Conclusion: Leukemia patients show different degrees of inheritance chromosome damages in the initial stage, indicating that the inheritance damage caused by chromosomal instability is related to leukemia pathogenesis.
DU Wei-jiao
,
YU Jin-pu
,
LI Hui
,
YANG Li-li
,
SHEN Chun
,
YU Wen-wen
,
XIN Ning
,
AN Xiu-mei
,
CAO Shui
,
REN Xiu-bao
2010, 17(5):545-548.
DOI: 10.3872/j.issn.1007-385X.2010.5.012
Abstract:
Objective:To examine the myeloid-derived suppressor cells (MDSCs) in breast cancer tissues and their relationship with clinicopathological characteristics of breast cancer. Methods: Thirty-five breast cancer samples were obtained from Tianjin Cancer Hospital (from Feb. 2009 to Dec. 2009), and single cell suspensions were prepared. The proportions of MDSCs（Lin-CD33+CD13+CD14-CD15-）in breast cancer tissues were determined by flow cytometry. Immunohistochemistry was used to detect the expressions of ER, PR, Her-2 proteins in the same tumor tissues. Then we analyzed the correlation of MDSCs ratio with clinical characteristics of breast cancer. Results:The MDSCs ratio in breast cancer tissues was correlated with the clinical stage and metastasis lymph node numbers in breast cancer patients, with the ratio in stage Ⅲ breast cancer patients (\[11.70±7.85\]%) being significantly higher than that in stage Ⅰ/Ⅱ patients (\[5.32±4.59\]%). Patients with more than 3 metastasis lymph nodes had a higher MDSCs ratio (\[10.97±7.87\]%) than patients with less than 3 metastasis lymph nodes (\[5.86±5.26\]%, P<0.05). MDSCs ratio was not correlated with ages, pathologic types, tumor diameters, histological grades, or expressions of ER, PR and Her-2 of breast cancer patients (P>0.05). Conclusion: The MDSCs ratio in breast cancer tissues is correlated with the clinical stage and lymph node metastasis of breast cancer, and the increased MDSCs numbers may be an important reason of immune suppression in breast cancer patients.
Objective:To examine the myeloid-derived suppressor cells (MDSCs) in breast cancer tissues and their relationship with clinicopathological characteristics of breast cancer. Methods: Thirty-five breast cancer samples were obtained from Tianjin Cancer Hospital (from Feb. 2009 to Dec. 2009), and single cell suspensions were prepared. The proportions of MDSCs（Lin-CD33+CD13+CD14-CD15-）in breast cancer tissues were determined by flow cytometry. Immunohistochemistry was used to detect the expressions of ER, PR, Her-2 proteins in the same tumor tissues. Then we analyzed the correlation of MDSCs ratio with clinical characteristics of breast cancer. Results:The MDSCs ratio in breast cancer tissues was correlated with the clinical stage and metastasis lymph node numbers in breast cancer patients, with the ratio in stage Ⅲ breast cancer patients (\[11.70±7.85\]%) being significantly higher than that in stage Ⅰ/Ⅱ patients (\[5.32±4.59\]%). Patients with more than 3 metastasis lymph nodes had a higher MDSCs ratio (\[10.97±7.87\]%) than patients with less than 3 metastasis lymph nodes (\[5.86±5.26\]%, P<0.05). MDSCs ratio was not correlated with ages, pathologic types, tumor diameters, histological grades, or expressions of ER, PR and Her-2 of breast cancer patients (P>0.05). Conclusion: The MDSCs ratio in breast cancer tissues is correlated with the clinical stage and lymph node metastasis of breast cancer, and the increased MDSCs numbers may be an important reason of immune suppression in breast cancer patients.
2010, 17(5):549-553.
DOI: 10.3872/j.issn.1007-385X.2010.5.013
Abstract:
Objective: To investigate the expressions of Syk (spleen tyrosine kinase), c-erbB-2 and epidermal growth factor receptor (EGFR) in gastric cardiac adenocarcinoma (GCA) and corresponding adjacent normal tissues, and to discuss their relationship with development and progression of GCA. Methods: Ninety-one GCA samples were obtained from the Fourth Hospital of Hebei Medical University (from Oct. 2006 to Dec. 2007). The expressions of Syk, c-erbB-2 and EGFR in GCA and corresponding adjacent normal tissues were determined by immunohistochemistry, and their correlations were analyzed. Results: The positive expression rate of Syk in GCA tissues was 24.18%, which was significantly lower than that in the adjacent normal tissues (60.44%, P<0.01). And the positive expression rates of c-erbB-2 and EGFR in GCA tissues were 56.04% and 58.24%, respectively, which were also higher than those in the adjacent normal tissues (P<0.01). The expressions of Syk and c-erbB-2 were correlated with pathology grade, lymphatic metastasis and TNM stage of GCA, and EGFR expression was only correlated with lymphatic metastasis. The expression of Syk was correlated with those of c-erbB-2 and EGFR (P<0.05), but Syk expression had no correlation with EGFR expression (P>0.05). Conclusion: Syk, c-erbB-2 and EGFR are abnormally expressed in GCA, which may contribute to pathogenesis of GCA. The combined detection of Syk, c-erbB-2 and EGFR may have potential significance in prognosis prediction of GCA.
Objective: To investigate the expressions of Syk (spleen tyrosine kinase), c-erbB-2 and epidermal growth factor receptor (EGFR) in gastric cardiac adenocarcinoma (GCA) and corresponding adjacent normal tissues, and to discuss their relationship with development and progression of GCA. Methods: Ninety-one GCA samples were obtained from the Fourth Hospital of Hebei Medical University (from Oct. 2006 to Dec. 2007). The expressions of Syk, c-erbB-2 and EGFR in GCA and corresponding adjacent normal tissues were determined by immunohistochemistry, and their correlations were analyzed. Results: The positive expression rate of Syk in GCA tissues was 24.18%, which was significantly lower than that in the adjacent normal tissues (60.44%, P<0.01). And the positive expression rates of c-erbB-2 and EGFR in GCA tissues were 56.04% and 58.24%, respectively, which were also higher than those in the adjacent normal tissues (P<0.01). The expressions of Syk and c-erbB-2 were correlated with pathology grade, lymphatic metastasis and TNM stage of GCA, and EGFR expression was only correlated with lymphatic metastasis. The expression of Syk was correlated with those of c-erbB-2 and EGFR (P<0.05), but Syk expression had no correlation with EGFR expression (P>0.05). Conclusion: Syk, c-erbB-2 and EGFR are abnormally expressed in GCA, which may contribute to pathogenesis of GCA. The combined detection of Syk, c-erbB-2 and EGFR may have potential significance in prognosis prediction of GCA.
2010, 17(5):554-558.
DOI: 10.3872/j.issn.1007-385X.2010.5.014
Abstract:
Objective:To observe the clinical effects and toxicity of gefitinib in treatment of patients with advanced non-small cell lung cancer (NSCLC) who failed to respond to prior chemotherapy. Methods: Sixty-four patients with advanced NSCLC were admitted to our hospital from Jun. 2005 to Aug. 2009. Gefitinib was given orally (250 mg) once daily to NSCLC patients until disease progression or the development of intolerable toxicity, and the clinical results were observed. Results: No patients showed complete response (CR), 22 patients showed partial response (PR), 23 patients maintained stable disease (SD), and 19 patients had disease progression (PD), with the overall response rate (CR+PR) being 34.38%, the stability disease rate being 35.94%, and disease control rate (CR+PR+SD) being 70.31%. The median survival period in our group was 5.9 months. Twenty-three patients of 64 (35.94％) were alive till the follow-up time. The effect of gefitinib was associated with gender and smoking (P<0.05), with better effect seen in females and non-smokers. The most common drug-related adverse events included grade ⅠorⅡ skin rash (32.81％, 26.57％) and diarrhea (12.5％). Conclusion:Gefitinib can relieve NCSLC-related symptoms in chemotherapy-resistant advanced NCSLC patients, especially in females and non-smokers; it is a safety, effective, and tolerable drug.
Objective:To observe the clinical effects and toxicity of gefitinib in treatment of patients with advanced non-small cell lung cancer (NSCLC) who failed to respond to prior chemotherapy. Methods: Sixty-four patients with advanced NSCLC were admitted to our hospital from Jun. 2005 to Aug. 2009. Gefitinib was given orally (250 mg) once daily to NSCLC patients until disease progression or the development of intolerable toxicity, and the clinical results were observed. Results: No patients showed complete response (CR), 22 patients showed partial response (PR), 23 patients maintained stable disease (SD), and 19 patients had disease progression (PD), with the overall response rate (CR+PR) being 34.38%, the stability disease rate being 35.94%, and disease control rate (CR+PR+SD) being 70.31%. The median survival period in our group was 5.9 months. Twenty-three patients of 64 (35.94％) were alive till the follow-up time. The effect of gefitinib was associated with gender and smoking (P<0.05), with better effect seen in females and non-smokers. The most common drug-related adverse events included grade ⅠorⅡ skin rash (32.81％, 26.57％) and diarrhea (12.5％). Conclusion:Gefitinib can relieve NCSLC-related symptoms in chemotherapy-resistant advanced NCSLC patients, especially in females and non-smokers; it is a safety, effective, and tolerable drug.
2010, 17(5):559-561.
DOI: 10.3872/j.issn.1007-385X.2010.5.015
Abstract:
目的：制备Cyclin D1b蛋白C端多肽的多克隆抗体，为后续Cyclin D1b的研究奠定基础。方法: 用生物信息学方法分析Cyclin D1b蛋白的同源性、亲水性和抗原性，设计并合成Cyclin D1b C端的氨基酸序列，将合成后的多肽与钥孔血蓝蛋白(Keyhole-limpet hemocyanin，KLH) 偶联并免疫新西兰大白兔，制备多克隆抗体。ELISA法检测多抗效价，Western blotting检测Cyclin D1b的表达，免疫组织化学法检测该抗体的特异性与适用范围。结果：成功制备兔抗人Cyclin D1b蛋白C端多肽的多克隆抗体，ELISA法效价为1∶18 000。纯化后的抗体用于Western blotting可特异识别MCF-7细胞中的Cyclin D1b，并可用于免疫组织化学检测。结论：制备成功Cyclin D1b蛋白C端多肽的多克隆抗体，此多抗可用于Western blotting和免疫组织化学等分析。
目的：制备Cyclin D1b蛋白C端多肽的多克隆抗体，为后续Cyclin D1b的研究奠定基础。方法: 用生物信息学方法分析Cyclin D1b蛋白的同源性、亲水性和抗原性，设计并合成Cyclin D1b C端的氨基酸序列，将合成后的多肽与钥孔血蓝蛋白(Keyhole-limpet hemocyanin，KLH) 偶联并免疫新西兰大白兔，制备多克隆抗体。ELISA法检测多抗效价，Western blotting检测Cyclin D1b的表达，免疫组织化学法检测该抗体的特异性与适用范围。结果：成功制备兔抗人Cyclin D1b蛋白C端多肽的多克隆抗体，ELISA法效价为1∶18 000。纯化后的抗体用于Western blotting可特异识别MCF-7细胞中的Cyclin D1b，并可用于免疫组织化学检测。结论：制备成功Cyclin D1b蛋白C端多肽的多克隆抗体，此多抗可用于Western blotting和免疫组织化学等分析。
2010, 17(5):562-564.
DOI: 10.3872/j.issn.1007-385X.2010.5.016
Abstract:
目的：探讨吉西他滨联合重组人血管内皮抑制素YH-16对裸鼠CD133+MHCC97H肝癌移植瘤中肝癌干细胞样细胞的影响。方法：用免疫磁珠分选MHCC97H中肝癌干细胞样细胞，将其接种到20只裸鼠皮下，建立移植瘤模型。治疗组给予吉西他滨和YH-16，对照组给予等量生理盐水，比较两组移植瘤大小变化及原代培养细胞球形成情况，流式细胞术检测原代培养中CD133+细胞百分率。结果：治疗组的移植瘤明显缩小，治疗组和对照组细胞球形成数目分别为(7.5±2.4)个 vs (16.0±3.5)个，细胞球直径分别为(178.30±19.21) μm vs (131.06±20.96) μm（P＜0.05）；治疗组和对照组原代培养中CD133+细胞百分数分别为（6.24±0.96）% vs（18.26±1.76）%（P＜0.05）。结论：低剂量吉西他滨联合YH-16可抑制血管内皮细胞破坏肝癌干细胞样细胞的血管巢，进而选择性清除肝癌干细胞样细胞。
目的：探讨吉西他滨联合重组人血管内皮抑制素YH-16对裸鼠CD133+MHCC97H肝癌移植瘤中肝癌干细胞样细胞的影响。方法：用免疫磁珠分选MHCC97H中肝癌干细胞样细胞，将其接种到20只裸鼠皮下，建立移植瘤模型。治疗组给予吉西他滨和YH-16，对照组给予等量生理盐水，比较两组移植瘤大小变化及原代培养细胞球形成情况，流式细胞术检测原代培养中CD133+细胞百分率。结果：治疗组的移植瘤明显缩小，治疗组和对照组细胞球形成数目分别为(7.5±2.4)个 vs (16.0±3.5)个，细胞球直径分别为(178.30±19.21) μm vs (131.06±20.96) μm（P＜0.05）；治疗组和对照组原代培养中CD133+细胞百分数分别为（6.24±0.96）% vs（18.26±1.76）%（P＜0.05）。结论：低剂量吉西他滨联合YH-16可抑制血管内皮细胞破坏肝癌干细胞样细胞的血管巢，进而选择性清除肝癌干细胞样细胞。
2010, 17(5):565-567.
DOI: 10.3872/j.issn.1007-385X.2010.5.017
Abstract:
目的：探讨手术后大肠癌患者外周血NKT细胞及NK细胞的变化及其影响因素。方法： 采集32例大肠癌患者手术前后和13例健康对照外周静脉血，流式细胞术检测外周血NKT及NK细胞的变化，研究其与大肠癌患者临床病理特征的关系。结果：大肠癌患者NKT细胞较健康人升高（P<0.05），T细胞与健康人无差异，NK细胞较健康人减少（P<0.05）。健康人群中NKT细胞占外周血T淋巴细胞的6.6%，低于大肠癌患者的18.9%（P<0.05）。术后1周，大肠癌患者NKT细胞较术前明显升高、NK细胞明显降低（P<0.05）。年龄＞60岁较年龄≤60的大肠癌患者的T细胞低（P<0.05）；有淋巴结转移患者的T细胞有降低趋势，NK细胞有增高趋势；肿瘤浸润至浆膜和浆膜外大肠癌患者T细胞有降低趋势；Duke’s C、D期较Duke’s A、B期大肠癌患者T细胞低（P<0.05）。T、NKT及NK细胞三者间无相关关系。结论：手术后大肠癌患者NKT细胞介导的抗肿瘤免疫反应处于活化状态，NK细胞处于抑制状态。
目的：探讨手术后大肠癌患者外周血NKT细胞及NK细胞的变化及其影响因素。方法： 采集32例大肠癌患者手术前后和13例健康对照外周静脉血，流式细胞术检测外周血NKT及NK细胞的变化，研究其与大肠癌患者临床病理特征的关系。结果：大肠癌患者NKT细胞较健康人升高（P<0.05），T细胞与健康人无差异，NK细胞较健康人减少（P<0.05）。健康人群中NKT细胞占外周血T淋巴细胞的6.6%，低于大肠癌患者的18.9%（P<0.05）。术后1周，大肠癌患者NKT细胞较术前明显升高、NK细胞明显降低（P<0.05）。年龄＞60岁较年龄≤60的大肠癌患者的T细胞低（P<0.05）；有淋巴结转移患者的T细胞有降低趋势，NK细胞有增高趋势；肿瘤浸润至浆膜和浆膜外大肠癌患者T细胞有降低趋势；Duke’s C、D期较Duke’s A、B期大肠癌患者T细胞低（P<0.05）。T、NKT及NK细胞三者间无相关关系。结论：手术后大肠癌患者NKT细胞介导的抗肿瘤免疫反应处于活化状态，NK细胞处于抑制状态。
2010, 17(5):568-570.
DOI: 10.3872/j.issn.1007-385X.2010.5.018
Abstract:
目的：比较3种简易形态观察法检测肝癌细胞凋亡的效果。方法：用6%的乙醇作用人肝细胞癌HCC-9204细胞6 h，诱导其凋亡，进行未固定细胞的吖啶橙/溴化乙啶(AO/EB)双染色、细胞固定后的H-E染色，以及TUNEL法检测肝癌细胞凋亡的形态学特征。结果：用6%乙醇诱导肝癌细胞凋亡后，AO/EB、H-E染色法以及TUNEL法均能够不同程度地显示细胞变圆、细胞核深染和染色质边集、呈环状、团块或新月体状，以及细胞质浓缩和“出泡”现象等细胞凋亡的典型形态学特征。AO/EB双染色法能够显示呈致密浓染的黄绿色染色或出现黄绿色碎片的早期凋亡细胞，还能显示呈致密红染或出现红色碎片的晚期凋亡细胞，也能显示呈红色膨大状的坏死细胞。结论：AO/EB双染色、细胞固定后的H-E染色，以及TUNEL法等3种方法均可不同程度地观察到凋亡细胞的形态学变化，其中的AO/EB双染色法还可以区分早期凋亡、晚期凋亡和坏死细胞，具有较大的实用价值。
目的：比较3种简易形态观察法检测肝癌细胞凋亡的效果。方法：用6%的乙醇作用人肝细胞癌HCC-9204细胞6 h，诱导其凋亡，进行未固定细胞的吖啶橙/溴化乙啶(AO/EB)双染色、细胞固定后的H-E染色，以及TUNEL法检测肝癌细胞凋亡的形态学特征。结果：用6%乙醇诱导肝癌细胞凋亡后，AO/EB、H-E染色法以及TUNEL法均能够不同程度地显示细胞变圆、细胞核深染和染色质边集、呈环状、团块或新月体状，以及细胞质浓缩和“出泡”现象等细胞凋亡的典型形态学特征。AO/EB双染色法能够显示呈致密浓染的黄绿色染色或出现黄绿色碎片的早期凋亡细胞，还能显示呈致密红染或出现红色碎片的晚期凋亡细胞，也能显示呈红色膨大状的坏死细胞。结论：AO/EB双染色、细胞固定后的H-E染色，以及TUNEL法等3种方法均可不同程度地观察到凋亡细胞的形态学变化，其中的AO/EB双染色法还可以区分早期凋亡、晚期凋亡和坏死细胞，具有较大的实用价值。
2010, 17(5):571-575.
DOI: 10.3872/j.issn.1007-385X.2010.5.019
Abstract:
Cancer stem cells (CSCs) are special stem cells recently found in many tumor tissues. CSCs are capable of self-renewal and differentiation. They can gradually differentiate into tumor cells and form new tumors; they can also be resistant to chemotherapy and radiotherapy, which may partly explain the recurrence and metastasis of tumors. CSCs can be used for diagnosis and treatment of tumors, since some tumors can be early diagnosed by detecting certain CSC markers. Some novel therapy strategies target signal transduction pathways, surface molecular markers and tumor microenvironments of CSCs, as well as induce differentiation of CSCs. Further insights into drug-resistance of CSCs and the identification of more CSCs markers may offer new therapeutic strategies for tumors.
Cancer stem cells (CSCs) are special stem cells recently found in many tumor tissues. CSCs are capable of self-renewal and differentiation. They can gradually differentiate into tumor cells and form new tumors; they can also be resistant to chemotherapy and radiotherapy, which may partly explain the recurrence and metastasis of tumors. CSCs can be used for diagnosis and treatment of tumors, since some tumors can be early diagnosed by detecting certain CSC markers. Some novel therapy strategies target signal transduction pathways, surface molecular markers and tumor microenvironments of CSCs, as well as induce differentiation of CSCs. Further insights into drug-resistance of CSCs and the identification of more CSCs markers may offer new therapeutic strategies for tumors.
2010, 17(5):576-578.
DOI: 10.3872/j.issn.1007-385X.2010.5.020
Abstract:
Toll-like receptors (TLRs) is a group of pattern recognition receptors which can sense pathogen invasion; by now 11 TLR members have been identified in the mammalian immune system. Of all these TLRs, TLR4 received the most attention from scientists. TLR4 is expressed in a verity of tumors, and TLR4 activation can promote the development and progression, apoptosis resistance, and invasion and metastasis of tumors. Besides, the exogenous activation and endogenous ligands in tumor microenvironment may also play important roles in tumor immune escape triggered by TLR4. TLR4 is expected to become a new target for cancer biotherapy.
Toll-like receptors (TLRs) is a group of pattern recognition receptors which can sense pathogen invasion; by now 11 TLR members have been identified in the mammalian immune system. Of all these TLRs, TLR4 received the most attention from scientists. TLR4 is expressed in a verity of tumors, and TLR4 activation can promote the development and progression, apoptosis resistance, and invasion and metastasis of tumors. Besides, the exogenous activation and endogenous ligands in tumor microenvironment may also play important roles in tumor immune escape triggered by TLR4. TLR4 is expected to become a new target for cancer biotherapy.
2010, 17(5):579-583.
DOI: 10.3872/j.issn.1007-385X.2010.5.021
Abstract:
Prostatitis is a risk factor of prostate cancer. Nuclear factor-κB (NF-κB) plays an important role in the tumorigenesis of prostate cancer induced by prostatitis. Hypoxia, a marker of inflammation, and Toll like receptors both can activate NF-κB. Inflammatory cells can regulate the biological behavior of tumors through NF-κB. Moreover, NF-κB has a cross-talk with many pro-inflammatory factors. NF-κB regulates tumor growth through various ways, including apoptosis promotion and proliferation suppression, mediation of invasion, metastasis and angiogenesis of tumors; NF-κB also can induce progression of prostate cancer from the androgen-dependent to the androgen-independent stage. Anti-inflammation and NF-κB-targeting therapies cast new lights on prostate cancer treatment, which deserves further study.
Prostatitis is a risk factor of prostate cancer. Nuclear factor-κB (NF-κB) plays an important role in the tumorigenesis of prostate cancer induced by prostatitis. Hypoxia, a marker of inflammation, and Toll like receptors both can activate NF-κB. Inflammatory cells can regulate the biological behavior of tumors through NF-κB. Moreover, NF-κB has a cross-talk with many pro-inflammatory factors. NF-κB regulates tumor growth through various ways, including apoptosis promotion and proliferation suppression, mediation of invasion, metastasis and angiogenesis of tumors; NF-κB also can induce progression of prostate cancer from the androgen-dependent to the androgen-independent stage. Anti-inflammation and NF-κB-targeting therapies cast new lights on prostate cancer treatment, which deserves further study.
2010, 17(5):584-588.
DOI: 10.3872/j.issn.1007-385X.2010.5.022
Abstract:
Prostate carcinoma (PC) is one of the most common male malignancies in Western countries, and recently the morbidity of PC have greatly increased in China. Bone morphogenetic proteins (BMPs) and their receptors (BMPRs) are expressed in prostate and PC tissues. BMPs can induce ectopic bone formation, cell chemotaxis, cell differentiation and embryogenesis. Some BMPs and BMPRs are expressed on PC cells and can be used as the prognostic markers for the development, progression and prognosis of PC. BMPs modulate the biological behaviors of PC cells in a diverse manner, depending on the cell type, cell differentiation state and local microenvironment. BMPs also play important roles in the progression of PC, especially in promoting PC metastasis to bone, accompanied by a strong osteoblastic reaction. Study on the relationship between BMPs and PC can help to explain the development and metastasis of PC, and provide a theoretical basis for PC therapy.
Prostate carcinoma (PC) is one of the most common male malignancies in Western countries, and recently the morbidity of PC have greatly increased in China. Bone morphogenetic proteins (BMPs) and their receptors (BMPRs) are expressed in prostate and PC tissues. BMPs can induce ectopic bone formation, cell chemotaxis, cell differentiation and embryogenesis. Some BMPs and BMPRs are expressed on PC cells and can be used as the prognostic markers for the development, progression and prognosis of PC. BMPs modulate the biological behaviors of PC cells in a diverse manner, depending on the cell type, cell differentiation state and local microenvironment. BMPs also play important roles in the progression of PC, especially in promoting PC metastasis to bone, accompanied by a strong osteoblastic reaction. Study on the relationship between BMPs and PC can help to explain the development and metastasis of PC, and provide a theoretical basis for PC therapy.
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- 《中国肿瘤生物治疗杂志》
- 1994年创刊
- 主办单位：Chinese Society of Immunology, Chinese Anti-cancer Association
- 邮编：200433
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- 网址:http://www.biother.cn
- 刊号：ISSN 1007-385X
- CN 31-1725/R
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.