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Volume 31,Issue 4,2024 Table of Contents
2024, 31(4):319-325.
DOI: 10.3872/j.issn.1007-385X.2024.04.001
Abstract:
In malignant tumor tissues, tumor-associated neutrophils (TANs) have become a crucial component of the tumor microenvironment. The role of TANs in tumors is multifaceted. On one hand, TANs can directly kill tumor cells or mediate the collaborative anti-tumor activities of other immune cells. On the other hand, TANs can promote tumor angiogenesis, extracellular matrix remodeling,and tumor cell immune evasion. The heterogeneity of these functions of TAN is formed under regulation by various mechanisms within the tumor microenvironment and plays an important role in tumor development or suppression, thus making it crucial to investigate the mechanisms underlying TAN heterogeneity and functional transitions in tumors and their potential clinical significance. These investigations not only help develop suppressive drugs and therapies targeting pro-tumor neutrophil subpopulations, but also further promote the establishment and screening of new evaluation standards for more immunotherapy beneficiary population groups.
In malignant tumor tissues, tumor-associated neutrophils (TANs) have become a crucial component of the tumor microenvironment. The role of TANs in tumors is multifaceted. On one hand, TANs can directly kill tumor cells or mediate the collaborative anti-tumor activities of other immune cells. On the other hand, TANs can promote tumor angiogenesis, extracellular matrix remodeling,and tumor cell immune evasion. The heterogeneity of these functions of TAN is formed under regulation by various mechanisms within the tumor microenvironment and plays an important role in tumor development or suppression, thus making it crucial to investigate the mechanisms underlying TAN heterogeneity and functional transitions in tumors and their potential clinical significance. These investigations not only help develop suppressive drugs and therapies targeting pro-tumor neutrophil subpopulations, but also further promote the establishment and screening of new evaluation standards for more immunotherapy beneficiary population groups.
SUN Lili
,
BAI Bing
,
YANG Xia
,
LI Yue
,
LI Yiquan
,
HAN Jicheng
,
FANG Jinbo
,
LI Xiao
,
SHANG Chao
,
ZHU Yilong
,
JIN Ningyi
2024, 31(4):326-332.
DOI: 10.3872/j.issn.1007-385X.2024.04.002
Abstract:
Objective: To explore the inhibitory effects and molecular mechanism of peiminine on colon cancer HCT116 cells.Methods: Human colon cancer HCT116 cells and normal colon epithelial CCD841 CON cells were treated with various concentrations of peiminine. The effects of peiminine on the proliferative vitality of HCT116 and CCD841 CON cells were detected by CCK-8 method and crystal violet staining. The effects of peiminine on the cell cycle and the expression of cycle related proteins in HCT116 cells were detected by flow cytometry and Western blot. HCT116 nude mouse transplantation tumor model and the AOM/DSS-induced colon cancer mouse model were constructed to observe the effects of peiminine on tumor growth and overall survival in the mouse model. The effects of peiminine on the expressions of cell cycle related proteins CDK4, CDK6 and cyclin D1 in transplanted tumors or tumor tissues were detected by immunohistochemistry and Western blot. Results: Peiminine significantly inhibited the proliferation ability (P<0.01), induced the G0/G1 phase arrest (P<0.01), and reduced the expression levels of CDK4, CDK6, and cyclin D1 proteins HCT116 cells (all P<0.01). The results of tumor bearing nude mice showed that peiminine (0.75 mg/kg) significantly inhibited the growth of HCT116 cell transplanted tumors, increased the overall survival rate (P<0.05 or P<0.01）. Peiminine also reduced the weight and prolonged the overall survival of AOM/DSS model mice, reduced the number and volume of tumors in cancerous colon tissues, and down-regulated the expressions of CDK4, CDK6 and cyclin D1 proteins in tumor tissues（P<0.05 or P<0.01）. Conclusion: Peiminine can cause cell cycle G0/G1 phase arrest, and thus suppress the proliferation of colon cancer HCT116 cells through downregulating the expression levels of CDK4, CDK6, and cyclin D1.
Objective: To explore the inhibitory effects and molecular mechanism of peiminine on colon cancer HCT116 cells.Methods: Human colon cancer HCT116 cells and normal colon epithelial CCD841 CON cells were treated with various concentrations of peiminine. The effects of peiminine on the proliferative vitality of HCT116 and CCD841 CON cells were detected by CCK-8 method and crystal violet staining. The effects of peiminine on the cell cycle and the expression of cycle related proteins in HCT116 cells were detected by flow cytometry and Western blot. HCT116 nude mouse transplantation tumor model and the AOM/DSS-induced colon cancer mouse model were constructed to observe the effects of peiminine on tumor growth and overall survival in the mouse model. The effects of peiminine on the expressions of cell cycle related proteins CDK4, CDK6 and cyclin D1 in transplanted tumors or tumor tissues were detected by immunohistochemistry and Western blot. Results: Peiminine significantly inhibited the proliferation ability (P<0.01), induced the G0/G1 phase arrest (P<0.01), and reduced the expression levels of CDK4, CDK6, and cyclin D1 proteins HCT116 cells (all P<0.01). The results of tumor bearing nude mice showed that peiminine (0.75 mg/kg) significantly inhibited the growth of HCT116 cell transplanted tumors, increased the overall survival rate (P<0.05 or P<0.01）. Peiminine also reduced the weight and prolonged the overall survival of AOM/DSS model mice, reduced the number and volume of tumors in cancerous colon tissues, and down-regulated the expressions of CDK4, CDK6 and cyclin D1 proteins in tumor tissues（P<0.05 or P<0.01）. Conclusion: Peiminine can cause cell cycle G0/G1 phase arrest, and thus suppress the proliferation of colon cancer HCT116 cells through downregulating the expression levels of CDK4, CDK6, and cyclin D1.
ZHU Zhiming
,
WANG Sumei
,
TANG Qing
,
WANG Xi
,
WAN Xinliang
,
MO Handan
,
JIA Luyu
,
YU Xiaoyan
,
ZHOU Qichun
2024, 31(4):333-341.
DOI: 10.3872/j.issn.1007-385X.2024.04.003
Abstract:
Objective: To explore the targets and potential mechanism of α-hederin (α-Hed) inducing cell apoptosis on non-small cell lung cancer (NSCLC), and to clarify the effects of α-Hed in combination with cisplatin (DDP) on the expression of target proteins. Methods: The viability of NSCLC cells (A549, H1299 and PC-9 cells) treated with different concentrations of α-Hed was detected by CCK-8 method.The apoptosis rate was determined by flow cytometry with Annexin Ⅴ-FITC/PI staining. The expressions of cleaved caspase-3 (C-caspase-3)and Bcl-2 proteins were detected by Western blot. The potential targets of α-Hed were screened by network pharmacology, and their binding effect was analyzed by molecular docking method. Besides, Western blot was applied to detect target protein expression. The suppressive effect of α-Hed in combination with DDP on NSCLC cells was detected by CCK-8 assay, colony formation assay and Western blot assay.Results: After 24 h and 48 h administration, α-Hed at 10, 15 and 20 μmol/L significantly inhibited the proliferation viability of NSCLC cells (all P<0.01). Compared with the control group, the apoptosis rate significantly increased after 20 μmol/L α-Hed treatment (P<0.01).C-caspase-3 expression in NSCLC cells was upregulated (P<0.05) and Bcl-2 expression was downregulated after α-Hed administration. The targets of AKT1, STAT3, EGFR and JAK2 with the binding affinity less than -5 kcal/mol were screened out via network pharmacology and molecular docking. Western blot showed that the expressions of EGFR, p-AKT/AKT, p-STAT3/STAT3 and JAK2 proteins in A549 and H1299 cells were significantly downregulated after α-Hed treatment (all P<0.05). Furthermore, α-Hed in combination with DDP more significantly inhibited the proliferation of NSCLC cells (P<0.01) and downregulated the expression of EGFR, p-AKT/AKT, p-STAT3/STAT3 and JAK2 proteins (P<0.05 or P<0.01). Conclusion: α-Hed induces the apoptosis of NSCLC by down-regulating EGFR and JAK2 expressions, and inhibiting the phosphorylation of STAT3 and AKT. Especially, the inhibitory effect is enhanced when α-Hed is used in combination with DDP, and the EGFR/AKT and JAK2/STAT3 pathways are further inhibited.
Objective: To explore the targets and potential mechanism of α-hederin (α-Hed) inducing cell apoptosis on non-small cell lung cancer (NSCLC), and to clarify the effects of α-Hed in combination with cisplatin (DDP) on the expression of target proteins. Methods: The viability of NSCLC cells (A549, H1299 and PC-9 cells) treated with different concentrations of α-Hed was detected by CCK-8 method.The apoptosis rate was determined by flow cytometry with Annexin Ⅴ-FITC/PI staining. The expressions of cleaved caspase-3 (C-caspase-3)and Bcl-2 proteins were detected by Western blot. The potential targets of α-Hed were screened by network pharmacology, and their binding effect was analyzed by molecular docking method. Besides, Western blot was applied to detect target protein expression. The suppressive effect of α-Hed in combination with DDP on NSCLC cells was detected by CCK-8 assay, colony formation assay and Western blot assay.Results: After 24 h and 48 h administration, α-Hed at 10, 15 and 20 μmol/L significantly inhibited the proliferation viability of NSCLC cells (all P<0.01). Compared with the control group, the apoptosis rate significantly increased after 20 μmol/L α-Hed treatment (P<0.01).C-caspase-3 expression in NSCLC cells was upregulated (P<0.05) and Bcl-2 expression was downregulated after α-Hed administration. The targets of AKT1, STAT3, EGFR and JAK2 with the binding affinity less than -5 kcal/mol were screened out via network pharmacology and molecular docking. Western blot showed that the expressions of EGFR, p-AKT/AKT, p-STAT3/STAT3 and JAK2 proteins in A549 and H1299 cells were significantly downregulated after α-Hed treatment (all P<0.05). Furthermore, α-Hed in combination with DDP more significantly inhibited the proliferation of NSCLC cells (P<0.01) and downregulated the expression of EGFR, p-AKT/AKT, p-STAT3/STAT3 and JAK2 proteins (P<0.05 or P<0.01). Conclusion: α-Hed induces the apoptosis of NSCLC by down-regulating EGFR and JAK2 expressions, and inhibiting the phosphorylation of STAT3 and AKT. Especially, the inhibitory effect is enhanced when α-Hed is used in combination with DDP, and the EGFR/AKT and JAK2/STAT3 pathways are further inhibited.
2024, 31(4):342-350.
DOI: 10.3872/j.issn.1007-385X.2024.04.004
Abstract:
Objective: To explore the role of nuclear receptor corepressor 2 (NCOR2) gene in the carcinogenesis and progression of esophageal squamous cell carcinoma (ESCC) and investigate its underlying molecular regulatory mechanism. Methods: Tumor tissue specimens, adjacent tissue specimens and clinical data of 155 ESCC patients diagnosed in Shanxi Tumor Hospital between May 2017 and July 2018 were collected. Transcriptome and clinicopathological data of patients were used for survival prognosis analysis and clinical association analysis. qPCR assay was conducted to detect the expression levels of NCOR2 gene in six ESCC cell lines (TE-1,TE-5, TE-9, KYSE150, KYSE180 and KYSE450). KYSE450 cells with highly-expressed NCOR2 gene were selected for siRNA knockdown experiment and construction of knockdown NCOR2 cell model. CCK-8 cell viability assay, colony formation assay, wound healing assay and Transwell assay were performed to explore the effect of NCOR2 knockdown on proliferation vitality, clone formation, invasion and migration abilities of KYSE450 cells. Transcriptome sequencing analysis was conducted on NCOR2 knockdown KYSE450 cells to identify differentially expressed genes. GO (Gene Ontology, GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes, KEGG) analysis were performed to characterize the signal regulation network that might be affected by NCOR2.Results: The expression of NCOR2 in ESCC tumor tissues was significantly higher than that in the adjacent tissues (P<0.01). Poor prognosis were associated with higher expression of NCOR2 in ESCC patients (P<0.05). The knocking-down of NCOR2 significantly reduced wound healing rate and cell migration and invasion abilities of KYSE450 cells (all P<0.01). However, cell proliferation and colony formation abilities were not significantly affected (all P>0.05). After NCOR2 knockdown in KYSE450 cells, transcriptome sequencing analysis revealed that 54 genes were significantly up-regulated and 127 genes were significantly down-regulated. KEGG analysis results showed that the significantly differentially expressed genes were enriched in PI3K/AKT signaling pathway (P<0.01). In the transcriptome data of the clinical samples of the 155 ESCC patients, the expression levels of the 4 genes PIK3R3, IL4R, COL1A1 and EFNA1 of the PI3K/AKT pathway were significantly correlated with NCOR2 (all P<0.01), which was consistent with the transcriptome sequencing analysis results. Conclusion: NCOR2 can promote the invasion and migration of KYSE450 cells via the PI3K/AKT signaling pathway, thus affecting ESCC carcinogenesis and progression.
Objective: To explore the role of nuclear receptor corepressor 2 (NCOR2) gene in the carcinogenesis and progression of esophageal squamous cell carcinoma (ESCC) and investigate its underlying molecular regulatory mechanism. Methods: Tumor tissue specimens, adjacent tissue specimens and clinical data of 155 ESCC patients diagnosed in Shanxi Tumor Hospital between May 2017 and July 2018 were collected. Transcriptome and clinicopathological data of patients were used for survival prognosis analysis and clinical association analysis. qPCR assay was conducted to detect the expression levels of NCOR2 gene in six ESCC cell lines (TE-1,TE-5, TE-9, KYSE150, KYSE180 and KYSE450). KYSE450 cells with highly-expressed NCOR2 gene were selected for siRNA knockdown experiment and construction of knockdown NCOR2 cell model. CCK-8 cell viability assay, colony formation assay, wound healing assay and Transwell assay were performed to explore the effect of NCOR2 knockdown on proliferation vitality, clone formation, invasion and migration abilities of KYSE450 cells. Transcriptome sequencing analysis was conducted on NCOR2 knockdown KYSE450 cells to identify differentially expressed genes. GO (Gene Ontology, GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes, KEGG) analysis were performed to characterize the signal regulation network that might be affected by NCOR2.Results: The expression of NCOR2 in ESCC tumor tissues was significantly higher than that in the adjacent tissues (P<0.01). Poor prognosis were associated with higher expression of NCOR2 in ESCC patients (P<0.05). The knocking-down of NCOR2 significantly reduced wound healing rate and cell migration and invasion abilities of KYSE450 cells (all P<0.01). However, cell proliferation and colony formation abilities were not significantly affected (all P>0.05). After NCOR2 knockdown in KYSE450 cells, transcriptome sequencing analysis revealed that 54 genes were significantly up-regulated and 127 genes were significantly down-regulated. KEGG analysis results showed that the significantly differentially expressed genes were enriched in PI3K/AKT signaling pathway (P<0.01). In the transcriptome data of the clinical samples of the 155 ESCC patients, the expression levels of the 4 genes PIK3R3, IL4R, COL1A1 and EFNA1 of the PI3K/AKT pathway were significantly correlated with NCOR2 (all P<0.01), which was consistent with the transcriptome sequencing analysis results. Conclusion: NCOR2 can promote the invasion and migration of KYSE450 cells via the PI3K/AKT signaling pathway, thus affecting ESCC carcinogenesis and progression.
2024, 31(4):351-358.
DOI: 10.3872/j.issn.1007-385X.2024.04.005
Abstract:
Objective: To investigate the effects of arctigenin (ARC) on the proliferation, apoptosis and invasion of oral squamous cell carcinoma (OSCC) HSC-3 cells by regulating the Notch/Hes-1 signaling pathway and its mechanism. Methods: Human HSC-3 cells were treated with different mass concentrations of ARC, and the effect of ARC on cell proliferation was detected by CCK-8 method to select the appropriate drug concentration. HSC-3 cells were divided into the control group, the ARC-L group (10 mg/L ARC), the ARC-M group (20 mg/L ARC), the ARC-H group (40 mg/L ARC), and the ARC-H+Jagged1/FC group (40 mg/L ARC+1.2 μg/mL Jagged1/FC).Cell proliferation ability was detected by EdU assay, and cell migration and invasion abilities, cell cycle and apoptosis rate were detected by scratch healing assay, Transwell assay and flow cytometry, respectively. The expression levels of proliferation (c-Myc,cyclin D1), apoptosis (BAX, Bcl-2, survivin), EMT (E-cadherin, vimentin, Snail) and Notch/Hes-1 pathway (Notch1, Hes-1, NICD)related proteins were detected by Western blot. Results: Compared with 0 mg/L, 10-80 mg/L of ARC significantly decreased the proliferation vitality of HSC-3 cells (all P<0.05). Compared with the control group, the EdU positive rate, scratch healing rate, invasion cell number, proportions of S phase and G2/M phase cells, and the expressions of c-Myc, cyclin D1, Bcl-2, survivin, vimentin, Snail, Notch 1, Hes-1, and NICD proteins of HSC-3 cells decreased significantly in the ARC-L, ARC-M, and ARC-H groups (all P<0.05); the apoptosis rate, the proportion of G0/G1 phase cells, and the expressions of BAX and E-cadherin proteins increased significantly (all P<0.05), and were concentration gradient dependent. Simultaneous use of Notch agonist Jagged1/FC partially reversed the effects of ARC on the proliferation, migration, invasion, apoptosis and the expressions of related proteins of HSC-3 cells (all P<0.05).Conclusion: ARC may inhibit the proliferation and invasion of OSCC HSC-3 cells and promote cell apoptosis by inhibiting the Notch/Hes-1 signaling pathway.
Objective: To investigate the effects of arctigenin (ARC) on the proliferation, apoptosis and invasion of oral squamous cell carcinoma (OSCC) HSC-3 cells by regulating the Notch/Hes-1 signaling pathway and its mechanism. Methods: Human HSC-3 cells were treated with different mass concentrations of ARC, and the effect of ARC on cell proliferation was detected by CCK-8 method to select the appropriate drug concentration. HSC-3 cells were divided into the control group, the ARC-L group (10 mg/L ARC), the ARC-M group (20 mg/L ARC), the ARC-H group (40 mg/L ARC), and the ARC-H+Jagged1/FC group (40 mg/L ARC+1.2 μg/mL Jagged1/FC).Cell proliferation ability was detected by EdU assay, and cell migration and invasion abilities, cell cycle and apoptosis rate were detected by scratch healing assay, Transwell assay and flow cytometry, respectively. The expression levels of proliferation (c-Myc,cyclin D1), apoptosis (BAX, Bcl-2, survivin), EMT (E-cadherin, vimentin, Snail) and Notch/Hes-1 pathway (Notch1, Hes-1, NICD)related proteins were detected by Western blot. Results: Compared with 0 mg/L, 10-80 mg/L of ARC significantly decreased the proliferation vitality of HSC-3 cells (all P<0.05). Compared with the control group, the EdU positive rate, scratch healing rate, invasion cell number, proportions of S phase and G2/M phase cells, and the expressions of c-Myc, cyclin D1, Bcl-2, survivin, vimentin, Snail, Notch 1, Hes-1, and NICD proteins of HSC-3 cells decreased significantly in the ARC-L, ARC-M, and ARC-H groups (all P<0.05); the apoptosis rate, the proportion of G0/G1 phase cells, and the expressions of BAX and E-cadherin proteins increased significantly (all P<0.05), and were concentration gradient dependent. Simultaneous use of Notch agonist Jagged1/FC partially reversed the effects of ARC on the proliferation, migration, invasion, apoptosis and the expressions of related proteins of HSC-3 cells (all P<0.05).Conclusion: ARC may inhibit the proliferation and invasion of OSCC HSC-3 cells and promote cell apoptosis by inhibiting the Notch/Hes-1 signaling pathway.
2024, 31(4):359-364.
DOI: 10.3872/j.issn.1007-385X.2024.04.006
Abstract:
Objective: To explore the effects of mesenchymal stem cell-derived exosomes (MSC-Exo) on the in vitro proliferation and migration of human colorectal cancer cells (CT26), and assess the effects and safety of MSC-Exo treatment for tumor-bearing mouse model with radiation enteritis (RE). Methods: Commercially available liquid dressing products containing MSC-Exo (MSC-Exo product) were utilized for this study. Exosome components were identified through Nanoparticle Tracking Analysis (NTA), transmission electron microscopy (TEM), and WB analysis. The effects of MSC-Exo product on CT26 cell proliferation and migration were detected using the CCK-8 and Transwell assays. A CT26 tumor-bearing mouse model was established, and the mice were intragastrically administered with 400 μL MSC-Exo product, MSC culture medium, or saline for 7 consecutive days to evaluate the effects of MSC-Exo product on tumor growth and mouse survival in vivo. A radiation enteritis tumor-bearing mouse model was also established, and administered similar treatments. The efficacy and safety of MSC-Exo product treatment for RE were evaluated through H-E staining of small intestine tissues. Results: NTA, TEM, and WB analyses confirmed the presence of MSC-Exo in the commercial liquid dressing products. In vitro studies showed that MSC-Exo product did not promote tumor proliferation or migration. In vitro studies revealed that MSC-Exo product did not promote the proliferation and migration of colon cancer CT26 cells and was thus safe. In vivo studies revealed that gavage administration of MSC-Exo product did not affect tumor growth and the survival period of tumor-bearing mice. However, after treating radiation enteritis tumor-bearing mouse model with MSC-Exo product via gavage, the symptoms of bloody and mucous stool were relieved. H-E staining results demonstrated improved tissue morphology integrity in the intestinal tissues of the mice compared with that of the mice in the control group, suggesting that MSC-Exo product was effective in treating RE in tumor-bearing mice and was safe in terms of oncogenicity and tumor metastasis. Conclusion: Commercial liquid dressing products containing MSC-Exo do not promote the proliferation and migration of colon cancer cells in vitro, and have no obvious effects on tumor growth and survival period of CT26 cell tumor-bearing mice, but are effective in treating RE in the tumor-bearing mouse model and improve intestinal tissue damage.
Objective: To explore the effects of mesenchymal stem cell-derived exosomes (MSC-Exo) on the in vitro proliferation and migration of human colorectal cancer cells (CT26), and assess the effects and safety of MSC-Exo treatment for tumor-bearing mouse model with radiation enteritis (RE). Methods: Commercially available liquid dressing products containing MSC-Exo (MSC-Exo product) were utilized for this study. Exosome components were identified through Nanoparticle Tracking Analysis (NTA), transmission electron microscopy (TEM), and WB analysis. The effects of MSC-Exo product on CT26 cell proliferation and migration were detected using the CCK-8 and Transwell assays. A CT26 tumor-bearing mouse model was established, and the mice were intragastrically administered with 400 μL MSC-Exo product, MSC culture medium, or saline for 7 consecutive days to evaluate the effects of MSC-Exo product on tumor growth and mouse survival in vivo. A radiation enteritis tumor-bearing mouse model was also established, and administered similar treatments. The efficacy and safety of MSC-Exo product treatment for RE were evaluated through H-E staining of small intestine tissues. Results: NTA, TEM, and WB analyses confirmed the presence of MSC-Exo in the commercial liquid dressing products. In vitro studies showed that MSC-Exo product did not promote tumor proliferation or migration. In vitro studies revealed that MSC-Exo product did not promote the proliferation and migration of colon cancer CT26 cells and was thus safe. In vivo studies revealed that gavage administration of MSC-Exo product did not affect tumor growth and the survival period of tumor-bearing mice. However, after treating radiation enteritis tumor-bearing mouse model with MSC-Exo product via gavage, the symptoms of bloody and mucous stool were relieved. H-E staining results demonstrated improved tissue morphology integrity in the intestinal tissues of the mice compared with that of the mice in the control group, suggesting that MSC-Exo product was effective in treating RE in tumor-bearing mice and was safe in terms of oncogenicity and tumor metastasis. Conclusion: Commercial liquid dressing products containing MSC-Exo do not promote the proliferation and migration of colon cancer cells in vitro, and have no obvious effects on tumor growth and survival period of CT26 cell tumor-bearing mice, but are effective in treating RE in the tumor-bearing mouse model and improve intestinal tissue damage.
2024, 31(4):365-370.
DOI: 10.3872/j.issn.1007-385X.2024.04.007
Abstract:
Objective: To investigate the effects of aucubin (AU) on epithelial interstitial transformation (EMT) and vasculogenic mimicry (VM) formation in gastric cancer MGC803 cells by regulating the RhoA/ROCK signaling pathway. Methods: Human gastric cancer MGC803 cells were routinely cultured and randomly divided into the Control group, the AU-L group (20 μmol/L AU), the AU-M group (40 μmol/L AU), the AU-H group (80 μmol/L AU), and the AU-H+RhoA activator naciclassine (Nar) group (AU-H+Nar group, 80 μmol/L AU+30 μmol/L Nar). The effects of AU on cell proliferation, invasion and migration were detected by CCK-8 assay, Transwell assay and cell scratch assay, respectively. Three-dimensional cell culture was applied to observe the effects of different concentration of AU on the formation of VM lumen in vitro in each group. The effects of different concentration of AU on the expressions of RhoA, ROCK, VM, and EMT related proteins in each group were detected by Western blot. Results: Compared with those in the Control group, the proliferation rates (48 and 72 h), the cell migration rate, the number of cell invasions, the number of VM lumen structures, the protein expressions of RhoA, ROCK1, N-cadherin, vimentin, and VE cadherin in MGC803 cells in the AU-M and AU-H groups reduced significantly (all P<0.05). The expression of E-cadherin increased significantly (P<0.05). Simultaneous use of Nar significantly weakened the inhibitory effect of AU on EMT and VM formation in MGC803 cells (all P<0.05). Conclusion: AU inhibits the proliferation, migration, invasion, EMT and VM formation processes of gastric cancer MGC803 cells by down-regulating the RhoA/ROCK signaling pathway.
Objective: To investigate the effects of aucubin (AU) on epithelial interstitial transformation (EMT) and vasculogenic mimicry (VM) formation in gastric cancer MGC803 cells by regulating the RhoA/ROCK signaling pathway. Methods: Human gastric cancer MGC803 cells were routinely cultured and randomly divided into the Control group, the AU-L group (20 μmol/L AU), the AU-M group (40 μmol/L AU), the AU-H group (80 μmol/L AU), and the AU-H+RhoA activator naciclassine (Nar) group (AU-H+Nar group, 80 μmol/L AU+30 μmol/L Nar). The effects of AU on cell proliferation, invasion and migration were detected by CCK-8 assay, Transwell assay and cell scratch assay, respectively. Three-dimensional cell culture was applied to observe the effects of different concentration of AU on the formation of VM lumen in vitro in each group. The effects of different concentration of AU on the expressions of RhoA, ROCK, VM, and EMT related proteins in each group were detected by Western blot. Results: Compared with those in the Control group, the proliferation rates (48 and 72 h), the cell migration rate, the number of cell invasions, the number of VM lumen structures, the protein expressions of RhoA, ROCK1, N-cadherin, vimentin, and VE cadherin in MGC803 cells in the AU-M and AU-H groups reduced significantly (all P<0.05). The expression of E-cadherin increased significantly (P<0.05). Simultaneous use of Nar significantly weakened the inhibitory effect of AU on EMT and VM formation in MGC803 cells (all P<0.05). Conclusion: AU inhibits the proliferation, migration, invasion, EMT and VM formation processes of gastric cancer MGC803 cells by down-regulating the RhoA/ROCK signaling pathway.
LI Xiongbing
,
ZHOU Ruifen
,
LI Jiali
,
WANG Hanjiao
,
WANG Chao
,
LI Jing
,
CAO Zhe
,
SHU Chengrong
2024, 31(4):371-376.
DOI: 10.3872/j.issn.1007-385X.2024.04.008
Abstract:
Objective: To investigate the therapeutic effect of programmed death-1 monoclonal antibody (PD-1 mAb) combined with cisplatin and gemcitabine in the treatment of transplanted tumor with KRAS gene mutant non-small cell lung cancer (NSCLC) A549 cells in mice.Methods: By constructing an immune system-tumor humanized mouse xenograft model with NSCLC A549 cells, 60 mice were randomly divided into 6 groups (10 mice/group), namely control group (200 μL/kg PBS), PD-1 mAb group (20 mg/kg PD-1 mAb), cisplatin group (3 mg/kg cisplatin), PD-1 mAb+cisplatin group (20 mg/kg PD-1 mAb+3 mg/kg cisplatin), gemcitabine group (30 mg/kg gemcitabine) and PD-1 mAb+gemcitabine group (20 mg/kg PD-1 mAb+30 mg/kg gemcitabine). TUNEL and DAPI double staining were used to detect the level of apoptosis in transplanted tumor tissues. The volume and mass of transplanted tumors were detected, and the growth inhibition rate of transplanted tumor was measured. The microvessel density (MVD) of transplanted tumor was determined by immunohistochemistry. Results: The humanized mouse xenograft model of NSCLC A549 cells was successfully constructed. Compared with the other five groups, the apoptosis rate and tumor growth inhibition rate in the PD-1 mAb+cisplatin group were the highest, and the tumor volume, mass, and MVD were the smallest (all P<0.05 ). Conclusion: Cisplatin has a synergistic activity with PD-1 mAb, while gemcitabine can antagonize the therapeutic effect of PD-1 mAb. It is suggested that PD-1 mAb combined with cisplatin chemotherapy is better for KRAS mutant NSCLC A549 cell transplanted tumor mice.
Objective: To investigate the therapeutic effect of programmed death-1 monoclonal antibody (PD-1 mAb) combined with cisplatin and gemcitabine in the treatment of transplanted tumor with KRAS gene mutant non-small cell lung cancer (NSCLC) A549 cells in mice.Methods: By constructing an immune system-tumor humanized mouse xenograft model with NSCLC A549 cells, 60 mice were randomly divided into 6 groups (10 mice/group), namely control group (200 μL/kg PBS), PD-1 mAb group (20 mg/kg PD-1 mAb), cisplatin group (3 mg/kg cisplatin), PD-1 mAb+cisplatin group (20 mg/kg PD-1 mAb+3 mg/kg cisplatin), gemcitabine group (30 mg/kg gemcitabine) and PD-1 mAb+gemcitabine group (20 mg/kg PD-1 mAb+30 mg/kg gemcitabine). TUNEL and DAPI double staining were used to detect the level of apoptosis in transplanted tumor tissues. The volume and mass of transplanted tumors were detected, and the growth inhibition rate of transplanted tumor was measured. The microvessel density (MVD) of transplanted tumor was determined by immunohistochemistry. Results: The humanized mouse xenograft model of NSCLC A549 cells was successfully constructed. Compared with the other five groups, the apoptosis rate and tumor growth inhibition rate in the PD-1 mAb+cisplatin group were the highest, and the tumor volume, mass, and MVD were the smallest (all P<0.05 ). Conclusion: Cisplatin has a synergistic activity with PD-1 mAb, while gemcitabine can antagonize the therapeutic effect of PD-1 mAb. It is suggested that PD-1 mAb combined with cisplatin chemotherapy is better for KRAS mutant NSCLC A549 cell transplanted tumor mice.
WANG Xiaoxiong
,
LI Quan
,
SHEN Zhenghai
,
CAI Jingjing
,
LI Zhuoying
,
SHEN Shaocong
,
LI Hongsheng
,
LIU Xin
,
LIU Xi
,
LIU Junxi
,
GUO Yinjin
,
DU Yaxi
,
LAN Yunyi
,
MA Luyao
,
YANG Ruijiao
,
WU Shunxian
,
ZHOU Yongchun
,
HUANG Yunchao
2024, 31(4):377-382.
DOI: 10.3872/j.issn.1007-385X.2024.04.009
Abstract:
Objective: To investigate the relationship between driver gene mutations and clinicopathological features of multi-nodular non-small cell lung cancer (NSCLC)，and to provide molecular diagnostic basis for the treatment of multi-nodular NSCLC patients. Methods: A total of 253 lung nodule tumor specimens from 121 patients with multiple nodules NSCLC tested at the Molecular Diagnostic Center of Yunnan Cancer Hospital between January 2018 and October 2023 were included in this study. Next-generation sequencing (NGS) or Amplification Refractory Mutation System PCR (ARMS-PCR) techniques were used to detect driver gene mutations in multi-nodular NSCLC tissues. The relationship between these mutations and clinical pathological features of patients was analyzed, in order to compare the tumor heterogeneity of lung cancer driver genes in different nodules. Results: Compared with non-"Xuanwei" NSCLC, "Xuanwei" multi-nodular NSCLC patients showed significant regional characteristics in driver gene mutations. These patients demonstrated a lower rate (20%) of epidermal growth factor receptor (EGFR) sensitive mutations (L858R, 19-del), a higher rate (27.26%) of EGFR rare mutations (mainly G719/S768I, G719). The KRAS mutation rate in "Xuanwei" multi-nodular NSCLC patients (27.27%) was also significantly higher than that in non- "Xuanwei" patients (12.59%) (P<0.05). In addition, the inconsistency rate of driver gene mutations among different nodules was 69.23% in "Xuanwei" multi-nodular NSCLC patients, much higher than that in non-"Xuanwei" patients (55.07%) (P<0.05). Conclusion: "Xuanwei" multi-nodular NSCLC patients in have higher EGFR rare mutations and KRAS mutation rates, and there is higher driver gene mutation heterogeneity among different lesions in the same patient. This study will provide more options for the diagnosis and treatment strategies of "Xuanwei" multi-nodular NSCLC.
Objective: To investigate the relationship between driver gene mutations and clinicopathological features of multi-nodular non-small cell lung cancer (NSCLC)，and to provide molecular diagnostic basis for the treatment of multi-nodular NSCLC patients. Methods: A total of 253 lung nodule tumor specimens from 121 patients with multiple nodules NSCLC tested at the Molecular Diagnostic Center of Yunnan Cancer Hospital between January 2018 and October 2023 were included in this study. Next-generation sequencing (NGS) or Amplification Refractory Mutation System PCR (ARMS-PCR) techniques were used to detect driver gene mutations in multi-nodular NSCLC tissues. The relationship between these mutations and clinical pathological features of patients was analyzed, in order to compare the tumor heterogeneity of lung cancer driver genes in different nodules. Results: Compared with non-"Xuanwei" NSCLC, "Xuanwei" multi-nodular NSCLC patients showed significant regional characteristics in driver gene mutations. These patients demonstrated a lower rate (20%) of epidermal growth factor receptor (EGFR) sensitive mutations (L858R, 19-del), a higher rate (27.26%) of EGFR rare mutations (mainly G719/S768I, G719). The KRAS mutation rate in "Xuanwei" multi-nodular NSCLC patients (27.27%) was also significantly higher than that in non- "Xuanwei" patients (12.59%) (P<0.05). In addition, the inconsistency rate of driver gene mutations among different nodules was 69.23% in "Xuanwei" multi-nodular NSCLC patients, much higher than that in non-"Xuanwei" patients (55.07%) (P<0.05). Conclusion: "Xuanwei" multi-nodular NSCLC patients in have higher EGFR rare mutations and KRAS mutation rates, and there is higher driver gene mutation heterogeneity among different lesions in the same patient. This study will provide more options for the diagnosis and treatment strategies of "Xuanwei" multi-nodular NSCLC.
2024, 31(4):383-391.
DOI: 10.3872/j.issn.1007-385X.2024.04.010
Abstract:
Objective:To analyze the expression level and clinical significance of Deltex E3 ubiquitin ligase 2 (DTX2) in clear cell renal cell carcinoma (ccRCC) based on TCGA database, and explore the effect of DTX2 on the proliferation, migration and invasion of ccRCC cells. Methods: TIMER database was utilized to analyze the expression level of DTX2 in pan-cancer tissues, while UALCAN database was used for further verification of the differences in mRNA and protein expressions of DTX2 in ccRCC and adjacent tissues. TCGA-ccRCC cohort dataset in UALCAN database was employed to examine the correlation between DTX2 expression in ccRCC and clinicopathological features of patients. The correlation between DTX2 expression and the prognosis of ccRCC patients was analyzed using K-M plot database. Using DAVID database, gene ontology (GO) analysis and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis were performed to explore DTX2-related genes. The expression levels of DTX2 gene in human embryonic kidney 293 (HEK293) cells and ccRCC A498 and Caki-1 cells were detected by qPCR. SiRNA technology was employed to transfect DTX2 siRNA and its negative control plasmids into ccRCC A498 and Caki-1 cells. CCK-8 cell proliferation assay, plate clone formation assay, scratch wound assay, and Transwell migration assay were performed to detect respectively the effects of knockdown DTX2 on the proliferation, migration and invasion of ccRCC cells. Results: Analysis of TCGA database showed that, compared with adjacent tissues, both DTX2 mRNA and protein were highly expressed in ccRCC tissues (all P<0.01). The expression level of DTX2 was associated with the pathological stage, clinical grade, different subtype, and lymph node metastasis of ccRCC patients (all P<0.01). High DTX2 expression was correlated with poor prognosis in patients (all P<0.01). The results of GO function analysis and KEGG pathway enrichment analysis and showed that genes related to DTX2 expression were mainly involved in biological processes such as proteasome-mediated ubiquitin-dependent protein catabolic process, and these genes were primarily enriched in tumor-related signaling pathways such as the mTOR signaling pathway (all P<0.05).The results of in vitro cell experiments showed that the expression levels of DTX2 in A498 and Caki-1 cells were higher than those in HEK293 cells; knockdown of DTX2 expression significantly lowered the proliferation, migration and invasion abilities of A498 and Caki-1 cells (all P<0.01). Conclusion: High expression of DTX2 is observed in ccRCC tissues and cells, and its high expression is associated with poor prognosis in patients. Knockdown of DTX2 expression may inhibit the proliferation, migration and invasion of ccRCC cells. DTX2 is expected to become a new biomarker and therapeutic target for ccRCC.
Objective:To analyze the expression level and clinical significance of Deltex E3 ubiquitin ligase 2 (DTX2) in clear cell renal cell carcinoma (ccRCC) based on TCGA database, and explore the effect of DTX2 on the proliferation, migration and invasion of ccRCC cells. Methods: TIMER database was utilized to analyze the expression level of DTX2 in pan-cancer tissues, while UALCAN database was used for further verification of the differences in mRNA and protein expressions of DTX2 in ccRCC and adjacent tissues. TCGA-ccRCC cohort dataset in UALCAN database was employed to examine the correlation between DTX2 expression in ccRCC and clinicopathological features of patients. The correlation between DTX2 expression and the prognosis of ccRCC patients was analyzed using K-M plot database. Using DAVID database, gene ontology (GO) analysis and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis were performed to explore DTX2-related genes. The expression levels of DTX2 gene in human embryonic kidney 293 (HEK293) cells and ccRCC A498 and Caki-1 cells were detected by qPCR. SiRNA technology was employed to transfect DTX2 siRNA and its negative control plasmids into ccRCC A498 and Caki-1 cells. CCK-8 cell proliferation assay, plate clone formation assay, scratch wound assay, and Transwell migration assay were performed to detect respectively the effects of knockdown DTX2 on the proliferation, migration and invasion of ccRCC cells. Results: Analysis of TCGA database showed that, compared with adjacent tissues, both DTX2 mRNA and protein were highly expressed in ccRCC tissues (all P<0.01). The expression level of DTX2 was associated with the pathological stage, clinical grade, different subtype, and lymph node metastasis of ccRCC patients (all P<0.01). High DTX2 expression was correlated with poor prognosis in patients (all P<0.01). The results of GO function analysis and KEGG pathway enrichment analysis and showed that genes related to DTX2 expression were mainly involved in biological processes such as proteasome-mediated ubiquitin-dependent protein catabolic process, and these genes were primarily enriched in tumor-related signaling pathways such as the mTOR signaling pathway (all P<0.05).The results of in vitro cell experiments showed that the expression levels of DTX2 in A498 and Caki-1 cells were higher than those in HEK293 cells; knockdown of DTX2 expression significantly lowered the proliferation, migration and invasion abilities of A498 and Caki-1 cells (all P<0.01). Conclusion: High expression of DTX2 is observed in ccRCC tissues and cells, and its high expression is associated with poor prognosis in patients. Knockdown of DTX2 expression may inhibit the proliferation, migration and invasion of ccRCC cells. DTX2 is expected to become a new biomarker and therapeutic target for ccRCC.
2024, 31(4):392-396.
DOI: 10.3872/j.issn.1007-385X.2024.04.011
Abstract:
卡波西肉瘤相关疱疹病毒（KSHV）是一种与多种类型人类恶性肿瘤密切相关的致癌γ疱疹病毒。KSHV相关肿瘤的抗病毒药物局限，患者对常用的抗病毒药物存在明显的异质性，且并不总是对KSHV诱发的疾病有效，因此亟需寻找不同分子机制的合适靶点来治疗KSHV 相关疾病。KSHV 通过基因及编码的致癌蛋白、信号通路直接或间接调控糖酵解代谢与氨基酸代谢，通过促进脂肪酸合成和过氧化物酶体对脂质代谢进行调控，进而促进KSHV潜伏裂解期病毒粒子复制、存活、转化和诱导血管生成等影响肿瘤的发生和治疗效果。此外，靶向KSHV诱导代谢过程中的基因、信号通路、代谢调节因子和代谢物在有关体内体外实验的研究中，有显著的抗病毒和抑瘤效果，表现出具有成为治疗靶点的潜力。对KSHV诱导代谢重编程的致瘤作用及机制的认识可以为其相关疾病的治疗提供理论依据。本文对KSHV诱导糖酵解代谢、氨基酸代谢和脂质代谢发生的异常改变和分子机制，以及基于KSHV诱导代谢重编程的相关潜在治疗靶点进行了综述。
卡波西肉瘤相关疱疹病毒（KSHV）是一种与多种类型人类恶性肿瘤密切相关的致癌γ疱疹病毒。KSHV相关肿瘤的抗病毒药物局限，患者对常用的抗病毒药物存在明显的异质性，且并不总是对KSHV诱发的疾病有效，因此亟需寻找不同分子机制的合适靶点来治疗KSHV 相关疾病。KSHV 通过基因及编码的致癌蛋白、信号通路直接或间接调控糖酵解代谢与氨基酸代谢，通过促进脂肪酸合成和过氧化物酶体对脂质代谢进行调控，进而促进KSHV潜伏裂解期病毒粒子复制、存活、转化和诱导血管生成等影响肿瘤的发生和治疗效果。此外，靶向KSHV诱导代谢过程中的基因、信号通路、代谢调节因子和代谢物在有关体内体外实验的研究中，有显著的抗病毒和抑瘤效果，表现出具有成为治疗靶点的潜力。对KSHV诱导代谢重编程的致瘤作用及机制的认识可以为其相关疾病的治疗提供理论依据。本文对KSHV诱导糖酵解代谢、氨基酸代谢和脂质代谢发生的异常改变和分子机制，以及基于KSHV诱导代谢重编程的相关潜在治疗靶点进行了综述。
2024, 31(4):397-403.
DOI: 10.3872/j.issn.1007-385X.2024.04.012
Abstract:
三阴性乳腺癌（TNBC）是最具侵袭性的乳腺癌亚型，PI3K/AKT/mTOR信号通路失调是TNBC 最常见的致癌突变之一，靶向PI3K/AKT/mTOR信号通路是治疗TNBC的重要方向。本文着重介绍了PI3K/AKT/mTOR信号通路的机制，TNBC中出现的PIK3CA、AKT1或mTOR的突变，以及失活张力PTEN、PIK3R1或INPP4B的突变或丢失，也展现了布帕尼西、帕他色替、依维莫司等PI3K/AKT/mTOR信号通路靶向药物在治疗TNBC中单独、联合应用和与化疗或免疫疗法联用的疗效，同时论述了目前正在进行的各类临床试验及其未来的前景。
三阴性乳腺癌（TNBC）是最具侵袭性的乳腺癌亚型，PI3K/AKT/mTOR信号通路失调是TNBC 最常见的致癌突变之一，靶向PI3K/AKT/mTOR信号通路是治疗TNBC的重要方向。本文着重介绍了PI3K/AKT/mTOR信号通路的机制，TNBC中出现的PIK3CA、AKT1或mTOR的突变，以及失活张力PTEN、PIK3R1或INPP4B的突变或丢失，也展现了布帕尼西、帕他色替、依维莫司等PI3K/AKT/mTOR信号通路靶向药物在治疗TNBC中单独、联合应用和与化疗或免疫疗法联用的疗效，同时论述了目前正在进行的各类临床试验及其未来的前景。
2024, 31(4):404-409.
DOI: 10.3872/j.issn.1007-385X.2024.04.013
Abstract:
澳洲茄碱（SS）是一种天然来源的生物活性小分子化合物，已经被证实具有抗菌、抗炎和抗肿瘤等功效。在抗肿瘤作用方面，SS可以通过多种机制在不同类型肿瘤中有效发挥抗肿瘤作用，其作用机制包括诱导肿瘤细胞凋亡、阻滞肿瘤细胞周期、诱导肿瘤细胞铁死亡、调控肿瘤相关非编码RNA、调节免疫和炎症反应、削弱肿瘤细胞的侵袭和转移能力、抑制糖酵解进程和肿瘤干细胞的产生等，涵盖了肺癌、肝癌、胃癌、乳腺癌、胆管癌、膀胱癌、胰腺癌、白血病、骨肉瘤等多种癌症类型。阐明SS 在不同类型肿瘤中的抗肿瘤活性及其作用机制，为促进SS 抗肿瘤作用机制的进一步研究和开发更有效安全的抗肿瘤药物提供了重要的理论基础。
澳洲茄碱（SS）是一种天然来源的生物活性小分子化合物，已经被证实具有抗菌、抗炎和抗肿瘤等功效。在抗肿瘤作用方面，SS可以通过多种机制在不同类型肿瘤中有效发挥抗肿瘤作用，其作用机制包括诱导肿瘤细胞凋亡、阻滞肿瘤细胞周期、诱导肿瘤细胞铁死亡、调控肿瘤相关非编码RNA、调节免疫和炎症反应、削弱肿瘤细胞的侵袭和转移能力、抑制糖酵解进程和肿瘤干细胞的产生等，涵盖了肺癌、肝癌、胃癌、乳腺癌、胆管癌、膀胱癌、胰腺癌、白血病、骨肉瘤等多种癌症类型。阐明SS 在不同类型肿瘤中的抗肿瘤活性及其作用机制，为促进SS 抗肿瘤作用机制的进一步研究和开发更有效安全的抗肿瘤药物提供了重要的理论基础。
2024, 31(4):410-415.
DOI: 10.3872/j.issn.1007-385X.2024.04.014
Abstract:
聚腺苷二磷酸核糖聚合酶（PARP）抑制剂可以显著提高患者生存期已用于卵巢癌的临床治疗，以PARP抑制剂为代表的卵巢癌维持治疗已成为卵巢癌治疗的热点话题。PARP抑制剂通过其合成致死作用极大延长了卵巢癌患者的无进展生存期和总生存期，但在治疗中有相当一部分卵巢癌患者对PARP抑制剂产生耐药，导致治疗效果不佳。目前国内外聚焦于研究PARP抑制剂的耐药及其抗耐药机制，通过与其他药物联合治疗等方法延缓甚至对抗PARP抑制剂的耐药。本文综述了近年来关于PARP抑制剂的临床耐药机制及其应对其耐药的方法，为提高临床医生对PARP抑制剂耐药性的认知和合理用药，增强 PARP抑制剂治疗的敏感性，以及提高卵巢癌临床治疗效果提供新的思路和研究方向。
聚腺苷二磷酸核糖聚合酶（PARP）抑制剂可以显著提高患者生存期已用于卵巢癌的临床治疗，以PARP抑制剂为代表的卵巢癌维持治疗已成为卵巢癌治疗的热点话题。PARP抑制剂通过其合成致死作用极大延长了卵巢癌患者的无进展生存期和总生存期，但在治疗中有相当一部分卵巢癌患者对PARP抑制剂产生耐药，导致治疗效果不佳。目前国内外聚焦于研究PARP抑制剂的耐药及其抗耐药机制，通过与其他药物联合治疗等方法延缓甚至对抗PARP抑制剂的耐药。本文综述了近年来关于PARP抑制剂的临床耐药机制及其应对其耐药的方法，为提高临床医生对PARP抑制剂耐药性的认知和合理用药，增强 PARP抑制剂治疗的敏感性，以及提高卵巢癌临床治疗效果提供新的思路和研究方向。
2024, 31(4):416-421.
DOI: 10.3872/j.issn.1007-385X.2024.04.015
Abstract:
近年来，中医药在恶性肿瘤的治疗中发挥重要作用。甘草是最常用的中药之一，主要活性成分为三萜皂苷类、黄酮类以及香豆素类物质。研究发现，甘草可通过介导肿瘤细胞凋亡和自噬、抑制肿瘤细胞增殖和转移等途径发挥抗肿瘤作用。目前，甘草相关方剂，如大黄甘草汤、补中益气汤和六君子汤等，在肿瘤辅助治疗中多有应用，可缓解肿瘤疼痛、黏膜刺激、胃肠道不良反应、贫血等。针对甘草抗肿瘤的主要有效成分异甘草素水溶性差、生物利用度低、体内半衰期短的问题，纳米悬浮液、脂质-聚合物杂化纳米颗粒系统和聚合物胶束等新型药物递送系统的研究突飞猛进。开发甘草及其生物活性成分作为抗肿瘤药物具有巨大潜力和应用价值。
近年来，中医药在恶性肿瘤的治疗中发挥重要作用。甘草是最常用的中药之一，主要活性成分为三萜皂苷类、黄酮类以及香豆素类物质。研究发现，甘草可通过介导肿瘤细胞凋亡和自噬、抑制肿瘤细胞增殖和转移等途径发挥抗肿瘤作用。目前，甘草相关方剂，如大黄甘草汤、补中益气汤和六君子汤等，在肿瘤辅助治疗中多有应用，可缓解肿瘤疼痛、黏膜刺激、胃肠道不良反应、贫血等。针对甘草抗肿瘤的主要有效成分异甘草素水溶性差、生物利用度低、体内半衰期短的问题，纳米悬浮液、脂质-聚合物杂化纳米颗粒系统和聚合物胶束等新型药物递送系统的研究突飞猛进。开发甘草及其生物活性成分作为抗肿瘤药物具有巨大潜力和应用价值。
2024, 31(4):422-424.
DOI: 10.3872/j.issn.1007-385X.2024.04.016
Abstract:
三阴性乳腺癌（TNBC）是最具侵袭性的乳腺癌亚型之一。化疗是目前转移性TNBC的主要治疗手段，但其疗效往往有限。免疫治疗能够避免由于肿瘤克隆进化带来的治疗抵抗，因而近年来成为多种类型肿瘤的治疗突破。尽管免疫检查点抑制剂（ICI）联合化疗被批准用于治疗PD-L1阳性TNBC，但是二线及以后疗效并不确切。本文报道了1例巨大髋骨转移接受紫杉醇联合铂类化疗耐药的TNBC病例，在使用放疗联合免疫治疗及抗血管生成药物安罗替尼的免疫综合治疗后，疗效评价达到部分缓解，患者生活质量明显改善。以放疗联合免疫治疗为基础的综合治疗模式有望成为晚期TNBC的有效治疗方案。
三阴性乳腺癌（TNBC）是最具侵袭性的乳腺癌亚型之一。化疗是目前转移性TNBC的主要治疗手段，但其疗效往往有限。免疫治疗能够避免由于肿瘤克隆进化带来的治疗抵抗，因而近年来成为多种类型肿瘤的治疗突破。尽管免疫检查点抑制剂（ICI）联合化疗被批准用于治疗PD-L1阳性TNBC，但是二线及以后疗效并不确切。本文报道了1例巨大髋骨转移接受紫杉醇联合铂类化疗耐药的TNBC病例，在使用放疗联合免疫治疗及抗血管生成药物安罗替尼的免疫综合治疗后，疗效评价达到部分缓解，患者生活质量明显改善。以放疗联合免疫治疗为基础的综合治疗模式有望成为晚期TNBC的有效治疗方案。
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.
Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.