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Volume 28,Issue 5,2021 Table of Contents
2021, 28(5):419-430.
DOI: 10.3872/j.issn.1007-385X.2021.05.001
Abstract:
[Abstract] In recent years, immune checkpoint inhibitors (ICIs), by enhancing the killing effect of the human immune system on tumor cells, have obtained significant clinical efficacy in anti-tumor therapy. However, sufficient evidence has shown that immunotherapy can lead to unique immune-related adverse events (irAEs) when activating the immune system, which can affect the efficacy of immunotherapy or discontinue the treatment. In recent years, with the wide development of clinical trials of immunotherapy, more and more attention has been paid to the occurrence, adverse events profiles, as well as the development of effective management approaches of irAEs. Common irAEs include dermatitis and thyroiditis, etc. The use of different types of ICIs, different therapeutic doses or combination therapies can lead to different irAEs profiles, even the use of same ICI on different types of tumors can cause different irAEs profiles. At present, it is believed that the occurrence of irAEs is related to the changes of immune system, including excessive activation of the immune system and the breakdown of autoimmune tolerance, but the specific mechanism is still not very clear. This review integrated the new advances that have been made in recent years in the key theory and understanding of exploring the molecular mechanisms and predictive markers associated with irAEs of ICIs therapy to summarize the occurrence characteristics and molecular mechanisms of irAEs. This review also provide an overview of predictive markers, improvement on management principles, as well as new explorations for the treatment of irAEs
[Abstract] In recent years, immune checkpoint inhibitors (ICIs), by enhancing the killing effect of the human immune system on tumor cells, have obtained significant clinical efficacy in anti-tumor therapy. However, sufficient evidence has shown that immunotherapy can lead to unique immune-related adverse events (irAEs) when activating the immune system, which can affect the efficacy of immunotherapy or discontinue the treatment. In recent years, with the wide development of clinical trials of immunotherapy, more and more attention has been paid to the occurrence, adverse events profiles, as well as the development of effective management approaches of irAEs. Common irAEs include dermatitis and thyroiditis, etc. The use of different types of ICIs, different therapeutic doses or combination therapies can lead to different irAEs profiles, even the use of same ICI on different types of tumors can cause different irAEs profiles. At present, it is believed that the occurrence of irAEs is related to the changes of immune system, including excessive activation of the immune system and the breakdown of autoimmune tolerance, but the specific mechanism is still not very clear. This review integrated the new advances that have been made in recent years in the key theory and understanding of exploring the molecular mechanisms and predictive markers associated with irAEs of ICIs therapy to summarize the occurrence characteristics and molecular mechanisms of irAEs. This review also provide an overview of predictive markers, improvement on management principles, as well as new explorations for the treatment of irAEs
2021, 28(5):431-434.
DOI: 10.3872/j.issn.1007-385X.2021.05.002
Abstract:
[Abstract] Clinical research on genetically engineered T cells has been carried out in China; however, there is no professional guidance for doctors to manage the treatment in such clinical research. Therefore, the Committee of Quality Control and Research of Cell Therapy, China Quality Association for Pharmaceuticals focuses on the specialty of clinical research of genetically engineered T cells, and organizes experts in the field to integrate the latest research progress and clinical practices, aiming to provide advices and suggestions on the selection of patients, the collection and preparation of cells, the storage and transportation of cells, as well as give recommendations on the clinical treatment before and after infusion and the evaluation of curative effects. After several rounds of discussion and revision, the Expert Guidance for Clinical Research of Genetically Engineered T Cells (2021) is finally formulated. This guidance aims to provide recommendations for clinical researchers and guard the safety and benefits of patients to the largest extent.
[Abstract] Clinical research on genetically engineered T cells has been carried out in China; however, there is no professional guidance for doctors to manage the treatment in such clinical research. Therefore, the Committee of Quality Control and Research of Cell Therapy, China Quality Association for Pharmaceuticals focuses on the specialty of clinical research of genetically engineered T cells, and organizes experts in the field to integrate the latest research progress and clinical practices, aiming to provide advices and suggestions on the selection of patients, the collection and preparation of cells, the storage and transportation of cells, as well as give recommendations on the clinical treatment before and after infusion and the evaluation of curative effects. After several rounds of discussion and revision, the Expert Guidance for Clinical Research of Genetically Engineered T Cells (2021) is finally formulated. This guidance aims to provide recommendations for clinical researchers and guard the safety and benefits of patients to the largest extent.
2021, 28(5):435-442.
DOI: 10.3872/j.issn.1007-385X.2021.05.003
Abstract:
[Abstract] Objective: To investigate the effects of silencing G protein-coupled receptor kinase 3 (GRK3) on the proliferation, migration and invasion of oral squamous cell carcinoma (OSCC) cells and the possible underlying mechanisms. Methods: GRK3 expression levels in normal oral tissues and OSCC tissues were analyzed using Oncomine database. RNA interference technology was used to down-regulate GRK3 expression in OSCC cell lines WSU-HN6 and CAL27. The interference efficiency was verified by qPCR. The effects of knockdown of GRK3 on proliferation and apoptosis of OSCC cells were detected by CCK-8 assay and Flow cytometry, respectively; the effects on migration and invasion abilities of OSCC cells were determined by Transwell assay; and the effects on mRNA expression levels of molecules associated with cell cycle, epithelial-mesenchymal transition (EMT), and matrix metallopeptidase (MMP) were determined by qPCR. The changes in protein levels of molecules associated with EMT and MMP were detected using WB assay. Results: GRK3 expression level in OSCC tissues was significantly higher than that in normal oral tissues ( P<0.01). After being transfected with si-GRK3, the mRNA expression of GRK3 in OSCC cells was down-regulated by more than 70%. Silencing GRK3 significantly inhibited the proliferation, migration and invasion of OSCC cells (all P<0.01), but had no significant effect on apoptosis (P>0.05). After down-regulation of GRK3, the percentage of OSCC cells in G0/G1 phase was significantly increased (P<0.01); the mRNA expression levels of Cyclin D1, Cyclin D3, CDK2 and CDK4 were decreased (all P<0.05); expression levels of EMT-related proteins (Vimentin, Zeb1 and Slug) were decreased, while E-cadherin was increased (all P<0.05); MMP3 and MMP9 were decreased (all P<0.05), while MMP2 and MMP7 showed no significant changes (all P>0.05). Conclusion: GRK3 promotes the proliferation of OSCC cells by regulating cell cycle-related molecules and enhances the migration and invasion through regulating EMT and MMPs.
[Abstract] Objective: To investigate the effects of silencing G protein-coupled receptor kinase 3 (GRK3) on the proliferation, migration and invasion of oral squamous cell carcinoma (OSCC) cells and the possible underlying mechanisms. Methods: GRK3 expression levels in normal oral tissues and OSCC tissues were analyzed using Oncomine database. RNA interference technology was used to down-regulate GRK3 expression in OSCC cell lines WSU-HN6 and CAL27. The interference efficiency was verified by qPCR. The effects of knockdown of GRK3 on proliferation and apoptosis of OSCC cells were detected by CCK-8 assay and Flow cytometry, respectively; the effects on migration and invasion abilities of OSCC cells were determined by Transwell assay; and the effects on mRNA expression levels of molecules associated with cell cycle, epithelial-mesenchymal transition (EMT), and matrix metallopeptidase (MMP) were determined by qPCR. The changes in protein levels of molecules associated with EMT and MMP were detected using WB assay. Results: GRK3 expression level in OSCC tissues was significantly higher than that in normal oral tissues ( P<0.01). After being transfected with si-GRK3, the mRNA expression of GRK3 in OSCC cells was down-regulated by more than 70%. Silencing GRK3 significantly inhibited the proliferation, migration and invasion of OSCC cells (all P<0.01), but had no significant effect on apoptosis (P>0.05). After down-regulation of GRK3, the percentage of OSCC cells in G0/G1 phase was significantly increased (P<0.01); the mRNA expression levels of Cyclin D1, Cyclin D3, CDK2 and CDK4 were decreased (all P<0.05); expression levels of EMT-related proteins (Vimentin, Zeb1 and Slug) were decreased, while E-cadherin was increased (all P<0.05); MMP3 and MMP9 were decreased (all P<0.05), while MMP2 and MMP7 showed no significant changes (all P>0.05). Conclusion: GRK3 promotes the proliferation of OSCC cells by regulating cell cycle-related molecules and enhances the migration and invasion through regulating EMT and MMPs.
2021, 28(5):443-450.
DOI: 10.3872/j.issn.1007-385X.2021.05.004
Abstract:
[Abstract] Objective: CRISPR/Cas9 technology was used to construct a stable transgenic strain of prostate cancer PC3 cells with TFDP3 gene knock-out (KO) to explore the effect of inhibiting TFDP3 expression on cell cycle, apoptosis and invasion of PC3 cells. Methods: The sgRNAs were screened by bioinformatics, and the sgRNA-cas9 co-transfection lentivirus with TFDP3 gene knockout was constructed by CRISPR/Cas9 technology. The constructed lentivirus was used to infect PC3 cells, and the stable transgenic strain was screened. Flow cytometry was used to detect the cell cycle distribution and apoptosis of cells in KO group (with TFDP3 KO) and control group. Cell migration and invasion capabilities were further detected by Scratch and Transwell assays. Results: Three sgRNAs were obtained through bioinformatics screening. Among them, the sgRNA2 obviously inhibited the prostate cancer gene expression. By using the CRISPR/Cas9 technology, a stable transgenic strain of PC3 prostate cancer cells with low expression of TFDP3 was obtained. The results of Flow cytometry showed that after the expression of TFDP3 gene was inhibited, compared with the control group, the percentage of cells in G0/G1 phase increased while the percentage of cells in G2/M stage decreased in the KO group, and the cell apoptosis rate significantly increased in the KO group (P<0.05); the migration rate of the PC3 cells in the KO group was significantly decreased (24 h migration rate: [44.00±1.60]% vs [65.00±4.40]%, P<0.01); the number of migrated cells in the KO group that passed through the polycarbonate membrane was significantly lower than that of the control group (185.89±11.71 vs 248.33±11.95, P<0.01). Conclusion: In this study, a stable transgenic strain of PC3 prostate cancer cell line with TFDP3 gene KO was constructed through CRISPR/Cas9 technology. It was confirmed that after the expression of TFDP3 gene was inhibited, PC3 cell cycle was blocked and the apoptosis rate was increased. Furthermore, the ability of migration and invasion was significantly weakened, suggesting that TFDP3 is a tumor-promoting gene in prostate cancer.
[Abstract] Objective: CRISPR/Cas9 technology was used to construct a stable transgenic strain of prostate cancer PC3 cells with TFDP3 gene knock-out (KO) to explore the effect of inhibiting TFDP3 expression on cell cycle, apoptosis and invasion of PC3 cells. Methods: The sgRNAs were screened by bioinformatics, and the sgRNA-cas9 co-transfection lentivirus with TFDP3 gene knockout was constructed by CRISPR/Cas9 technology. The constructed lentivirus was used to infect PC3 cells, and the stable transgenic strain was screened. Flow cytometry was used to detect the cell cycle distribution and apoptosis of cells in KO group (with TFDP3 KO) and control group. Cell migration and invasion capabilities were further detected by Scratch and Transwell assays. Results: Three sgRNAs were obtained through bioinformatics screening. Among them, the sgRNA2 obviously inhibited the prostate cancer gene expression. By using the CRISPR/Cas9 technology, a stable transgenic strain of PC3 prostate cancer cells with low expression of TFDP3 was obtained. The results of Flow cytometry showed that after the expression of TFDP3 gene was inhibited, compared with the control group, the percentage of cells in G0/G1 phase increased while the percentage of cells in G2/M stage decreased in the KO group, and the cell apoptosis rate significantly increased in the KO group (P<0.05); the migration rate of the PC3 cells in the KO group was significantly decreased (24 h migration rate: [44.00±1.60]% vs [65.00±4.40]%, P<0.01); the number of migrated cells in the KO group that passed through the polycarbonate membrane was significantly lower than that of the control group (185.89±11.71 vs 248.33±11.95, P<0.01). Conclusion: In this study, a stable transgenic strain of PC3 prostate cancer cell line with TFDP3 gene KO was constructed through CRISPR/Cas9 technology. It was confirmed that after the expression of TFDP3 gene was inhibited, PC3 cell cycle was blocked and the apoptosis rate was increased. Furthermore, the ability of migration and invasion was significantly weakened, suggesting that TFDP3 is a tumor-promoting gene in prostate cancer.
2021, 28(5):451-459.
DOI: 10.3872/j.issn.1007-385X.2021.05.005
Abstract:
[Abstract] Objective: To explore the effect of fibroblast growth factor13 (FGF13) on the generation of reactive oxygen species (ROS) and apoptosis of non-small cell lung cancer A549 cells and its regulatory mechanism. Methods: WB was used to detect the background expression of FGF13 in human normal lung epithelial BEAS-2B cells and lung cancer A549 and H460 cells. BEAS-2B and A549 cells were transfected with FGF13 over-expression vector. Two groups of shRNA sequences targeting FGF13 were designed to construct lentivirus interference vector. The packaged lentivirus was used to infect A549 cells. qPCR and WB were used to detect the interference efficiency. DCFH-DA probe combined with fluorescence microplate reader was used to analyze the effect of FGF13 knock-down on the level of ROS in A549 cells. MitoSOX and WB were used to detect mitochondrial ROS levels and nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) protein expression levels. Annexin V-FITC-PI double staining method was used to detect the cell apoptosis and expressions of Caspase-3 and Cleaved Caspase-3 protein. Results: FGF13 protein was highly expressed in lung cancer cells compared with BEAS-2B cells (both P<0.05). A549 cell line with over-expression and low-expression of FGF13 were successfully constructed. Over-expression of FGF13 significantly reduced the level of ROS in A549 and BEAS-2B cells (P<0.05), while knockdown of FGF13 significantly increased the level of ROS in A549 cells (P<0.05). Though over-expression and interference of FGF13 had no significant effect on mitochondrial ROS levels in A549 cells, NOX4 protein expression was significantly down-regulated (P<0.05) after FGF13 over-expression and significantly upregulated after FGF13 knockdown (P<0.05), respectively. The interference of FGF13 significantly increased the apoptosis rate (P<0.01) of A549 cells and significantly upregulated the protein expression levels of Caspase-3 and Cleaved Caspase-3 (P<0.05). Conclusion: FGF13 regulates ROS production possibly through the NOX family pathway and regulates apoptosis of A549 cells by the ROS/Caspase-3 pathway.
[Abstract] Objective: To explore the effect of fibroblast growth factor13 (FGF13) on the generation of reactive oxygen species (ROS) and apoptosis of non-small cell lung cancer A549 cells and its regulatory mechanism. Methods: WB was used to detect the background expression of FGF13 in human normal lung epithelial BEAS-2B cells and lung cancer A549 and H460 cells. BEAS-2B and A549 cells were transfected with FGF13 over-expression vector. Two groups of shRNA sequences targeting FGF13 were designed to construct lentivirus interference vector. The packaged lentivirus was used to infect A549 cells. qPCR and WB were used to detect the interference efficiency. DCFH-DA probe combined with fluorescence microplate reader was used to analyze the effect of FGF13 knock-down on the level of ROS in A549 cells. MitoSOX and WB were used to detect mitochondrial ROS levels and nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) protein expression levels. Annexin V-FITC-PI double staining method was used to detect the cell apoptosis and expressions of Caspase-3 and Cleaved Caspase-3 protein. Results: FGF13 protein was highly expressed in lung cancer cells compared with BEAS-2B cells (both P<0.05). A549 cell line with over-expression and low-expression of FGF13 were successfully constructed. Over-expression of FGF13 significantly reduced the level of ROS in A549 and BEAS-2B cells (P<0.05), while knockdown of FGF13 significantly increased the level of ROS in A549 cells (P<0.05). Though over-expression and interference of FGF13 had no significant effect on mitochondrial ROS levels in A549 cells, NOX4 protein expression was significantly down-regulated (P<0.05) after FGF13 over-expression and significantly upregulated after FGF13 knockdown (P<0.05), respectively. The interference of FGF13 significantly increased the apoptosis rate (P<0.01) of A549 cells and significantly upregulated the protein expression levels of Caspase-3 and Cleaved Caspase-3 (P<0.05). Conclusion: FGF13 regulates ROS production possibly through the NOX family pathway and regulates apoptosis of A549 cells by the ROS/Caspase-3 pathway.
2021, 28(5):460-468.
DOI: 10.3872/j.issn.1007-385X.2021.05.006
Abstract:
[Abstract] Objective: To identify the effect of circRNA circ_0091579 on the proliferation, apoptosis and invasion of colorectal cancer (CRC) cells by functioning as a molecular sponge of miR-330-3p and mediating ring finger protein 126 (RNF126). Methods: Sixty pairs of cancer tissue and adjacent normal tissue of CRC patients receiving surgical treatment in the First Affiliated Hospital of Dali University from February 2019 to May 2020 were collected. CRC LoVo cells with over-expression or knockdown of circ_0091579 and miR-330-3p were constructed. The expression of circ_0091579, miR-330-3p and RNF126 in CRC tissue and cell lines (HCT116, SW620, CW-2 and LoVo cells) was detected by qPCR. The proliferation, invasion and apoptosis were measured by MTT assay, Transwell assay and Flow cytometry, respectively. The targeting relationship between circ_0091579 and miR-330-3p, miR-330-3p and RNF126 was predicted by bioinformatics tool and verified by Dual luciferase reporter assay and RNA immunoprecipitation experiments. Results: In CRC tissues and cell lines, circ_0091579 and RNF126 were both highly expressed, and miR-330-3p was lowly expressed (all P＜ 0.05). Knockdown of circ_0091579 could inhibit the proliferation and invasion, but promote the apoptosis of CRC cells ( P＜ 0.05); however, this effect was reversed by miR-330-3p-inhibitor. Over-expression of miR-330-3p could suppress the ability of proliferation and invasion, but enhance the apoptosis of LoVo cells ( P＜0.05), and this effect was rescued after the participation of RNF126. There is a targeting relationship among circ_0091579, miR-330-3p and RNF126. Conclusion: circ_0091579 promotes the proliferation and invasion, and inhibits the apoptosis of LoVo cells via miR-330-3p/RNF126 axis.
[Abstract] Objective: To identify the effect of circRNA circ_0091579 on the proliferation, apoptosis and invasion of colorectal cancer (CRC) cells by functioning as a molecular sponge of miR-330-3p and mediating ring finger protein 126 (RNF126). Methods: Sixty pairs of cancer tissue and adjacent normal tissue of CRC patients receiving surgical treatment in the First Affiliated Hospital of Dali University from February 2019 to May 2020 were collected. CRC LoVo cells with over-expression or knockdown of circ_0091579 and miR-330-3p were constructed. The expression of circ_0091579, miR-330-3p and RNF126 in CRC tissue and cell lines (HCT116, SW620, CW-2 and LoVo cells) was detected by qPCR. The proliferation, invasion and apoptosis were measured by MTT assay, Transwell assay and Flow cytometry, respectively. The targeting relationship between circ_0091579 and miR-330-3p, miR-330-3p and RNF126 was predicted by bioinformatics tool and verified by Dual luciferase reporter assay and RNA immunoprecipitation experiments. Results: In CRC tissues and cell lines, circ_0091579 and RNF126 were both highly expressed, and miR-330-3p was lowly expressed (all P＜ 0.05). Knockdown of circ_0091579 could inhibit the proliferation and invasion, but promote the apoptosis of CRC cells ( P＜ 0.05); however, this effect was reversed by miR-330-3p-inhibitor. Over-expression of miR-330-3p could suppress the ability of proliferation and invasion, but enhance the apoptosis of LoVo cells ( P＜0.05), and this effect was rescued after the participation of RNF126. There is a targeting relationship among circ_0091579, miR-330-3p and RNF126. Conclusion: circ_0091579 promotes the proliferation and invasion, and inhibits the apoptosis of LoVo cells via miR-330-3p/RNF126 axis.
2021, 28(5):469-476.
DOI: 10.3872/j.issn.1007-385X.2021.05.007
Abstract:
[Abstract] Objective: To explore the biological function and mechanism of circular RNA (circRNA) 0072088 in non-small cell lung cancer (NSCLC) cells. Method: GSE101684 data set was downloaded from Gene Expression Omnibus (GEO), and the differentially expressed genes (DEGs) were screened with GEO2R analysis. The expression of circ_0072088 in NSCLC cell lines (H165， H358， H460， H226 and A549 cells) was detected using qPCR. CCK-8 assay and Transwell chamber assays were utilized to assess cell proliferation, migration and invasion. CircInteractome and TargetScan database were used to predict the targeting relationship between circ_0072088 and miR-545-3p as well as between miR-545-3p and STAT3, which were then verified by Dual luciferase reporter gene experiment and RNA binding protein immunoprecipitation (RIP) experiment. Results: The expression of circ_0072088 in NSCLC cell lines was significantly up-regulated (P <0.05). Over-expression of circ_0072088 promoted the proliferation, invasion and migration of NSCLC cells (P <0.05); knockdown of circ_ 0072088 inhibited the proliferation, invasion and migration of NSCLC cells (P <0.05). MiR-545-3p is the downstream target of circ_0072088 and can be sponged by circ_0072088; STAT3 is the target gene of miR-545-3p, which can be indirectly and positively regulated by circ_0072088. Conclusion: Circ_0072088 promotes the proliferation and metastasis of NSCLC cells by regulating the miR-545-3p /STAT3 axis.
[Abstract] Objective: To explore the biological function and mechanism of circular RNA (circRNA) 0072088 in non-small cell lung cancer (NSCLC) cells. Method: GSE101684 data set was downloaded from Gene Expression Omnibus (GEO), and the differentially expressed genes (DEGs) were screened with GEO2R analysis. The expression of circ_0072088 in NSCLC cell lines (H165， H358， H460， H226 and A549 cells) was detected using qPCR. CCK-8 assay and Transwell chamber assays were utilized to assess cell proliferation, migration and invasion. CircInteractome and TargetScan database were used to predict the targeting relationship between circ_0072088 and miR-545-3p as well as between miR-545-3p and STAT3, which were then verified by Dual luciferase reporter gene experiment and RNA binding protein immunoprecipitation (RIP) experiment. Results: The expression of circ_0072088 in NSCLC cell lines was significantly up-regulated (P <0.05). Over-expression of circ_0072088 promoted the proliferation, invasion and migration of NSCLC cells (P <0.05); knockdown of circ_ 0072088 inhibited the proliferation, invasion and migration of NSCLC cells (P <0.05). MiR-545-3p is the downstream target of circ_0072088 and can be sponged by circ_0072088; STAT3 is the target gene of miR-545-3p, which can be indirectly and positively regulated by circ_0072088. Conclusion: Circ_0072088 promotes the proliferation and metastasis of NSCLC cells by regulating the miR-545-3p /STAT3 axis.
2021, 28(5):477-481.
DOI: 10.3872/j.issn.1007-385X.2021.05.008
Abstract:
[Abstract] Objective: To investigate the effect of Enterococcus faecalis lipoteichoic acid (LTA) on the proliferation, invasion and migration of pancreatic ductal adenocarcinoma (PDA) cell line BxPC-3 and its possible mechanism. Methods: BxPC-3 cells were treated with 0, 5, 10 and 50 μg/ml LTA; the 0 μg/ml group was set as the blank control group, while the other groups were used as the experimental groups. CCK-8 method was used to detect the effect of LTA on the proliferation of BxPC-3 cells. BxPC-3 cells were treated with 50 μg/ml LTA for 48 h, and the invasion and migration abilities of BxPC-3 cells were detected by the Scratch test and Transwell chamber test, respectively. WB assay was used to detect the effect of LTA on protein expression of TLR2, P38, p-P38, NF-κB and p-NF-κB in BxPC-3 cells. Results: LTA inhibited the proliferation of BxPC-3 cells, and the inhibitory effect increased with time and concentration. Compared with the 0 μg/ml group, LTA at 50 μg/ml exhibited the most significant inhibitory effect on proliferation of BxPC-3 cells after 48 h (P<0.01); thus, the subsequent experimental groups were treated with 50 μg/ml LTA for 48 h. Compared with the 0 μg/ml group, the number of invaded cells and the migration rate of BxPC-3 cells in the 50 μg/ml group were significantly reduced (all P<0.01), and the protein expression levels of TLR2, p-P38 and p-NF-κB were significantly increased (all P<0.01). Conclusion: Enterococcus faecalis LTA can inhibit the proliferation, invasion and migration of pancreatic cancer BxPC-3 cells. The mechanism may be related to the activation of TLR2 by LTA to promote phosphorylation of P38 and NF-κB.
[Abstract] Objective: To investigate the effect of Enterococcus faecalis lipoteichoic acid (LTA) on the proliferation, invasion and migration of pancreatic ductal adenocarcinoma (PDA) cell line BxPC-3 and its possible mechanism. Methods: BxPC-3 cells were treated with 0, 5, 10 and 50 μg/ml LTA; the 0 μg/ml group was set as the blank control group, while the other groups were used as the experimental groups. CCK-8 method was used to detect the effect of LTA on the proliferation of BxPC-3 cells. BxPC-3 cells were treated with 50 μg/ml LTA for 48 h, and the invasion and migration abilities of BxPC-3 cells were detected by the Scratch test and Transwell chamber test, respectively. WB assay was used to detect the effect of LTA on protein expression of TLR2, P38, p-P38, NF-κB and p-NF-κB in BxPC-3 cells. Results: LTA inhibited the proliferation of BxPC-3 cells, and the inhibitory effect increased with time and concentration. Compared with the 0 μg/ml group, LTA at 50 μg/ml exhibited the most significant inhibitory effect on proliferation of BxPC-3 cells after 48 h (P<0.01); thus, the subsequent experimental groups were treated with 50 μg/ml LTA for 48 h. Compared with the 0 μg/ml group, the number of invaded cells and the migration rate of BxPC-3 cells in the 50 μg/ml group were significantly reduced (all P<0.01), and the protein expression levels of TLR2, p-P38 and p-NF-κB were significantly increased (all P<0.01). Conclusion: Enterococcus faecalis LTA can inhibit the proliferation, invasion and migration of pancreatic cancer BxPC-3 cells. The mechanism may be related to the activation of TLR2 by LTA to promote phosphorylation of P38 and NF-κB.
2021, 28(5):482-488.
DOI: 10.3872/j.issn.1007-385X.2021.05.009
Abstract:
[Abstract] Objective: To analyze the expression of Claudin-2 in human esophageal squamous cell carcinoma (ESCC) tissues and its relationship with clinicopathological characteristics and 5-year survival rate of ESCC patients, and to explore its effect on proliferation, migration and invasion of ESCC KYSE450 cells. Methods: A total of 52 cases of tumor tissues and 20 cases of corresponding para-cancerous tissues that surgically removed from ESCC patients who were primarily treated in Henan Cancer Hospital from 2010 to 2013 were collected for this study. Claudin-2 expression was analyzed by Immunohistochemistry and WB assay, and its relationship with clinicopathological characteristics and 5-year survival rate of ESCC patients was further investigated. The expression of Claudin-2 in ESCC cells (KYSE450, KYSE150, KYSE510 and KYSE140) and human immortalized esophageal epithelial SHEE cells was detected by WB assay. The Claudin-2 shRNA lentiviral vector was established and transfected into KYSE450 cells to establish a Claudin-2 knockdown cell line. Furthermore, the effects of knockdown of Claudin-2 on the proliferation, migration and invasion of KYSE450 cells were tested by clone formation experiment, cell scratch experiment and Transwell experiment. Results: The positive rate of Claudin-2 in ESCC tissues was significantly higher than that in adjacent tissues (P<0.05). The expression of Claudin-2 in ESCC tissues was related to lymph node metastasis (P<0.05). The 5-year survival rate of Claudin-2 positive patients was significantly lower than that of negative patients (P<0.05). The KYSE450 cell line with Claudin-2 knockdown was successfully constructed. The number of clone formation, wound healing rate and number of invaded cells in the sh-Claudin-2 group were significantly lower than those in the sh-NT group and the control group (all P<0.05). Conclusion: The expression level of Claudin-2 in ESCC tissues is higher than that of the tumor-adjacent tissues, and is negatively related with 5-year survival rate of ESCC patients. Claudin-2 can promote the proliferation, migration and invasion of ESCC cells.
[Abstract] Objective: To analyze the expression of Claudin-2 in human esophageal squamous cell carcinoma (ESCC) tissues and its relationship with clinicopathological characteristics and 5-year survival rate of ESCC patients, and to explore its effect on proliferation, migration and invasion of ESCC KYSE450 cells. Methods: A total of 52 cases of tumor tissues and 20 cases of corresponding para-cancerous tissues that surgically removed from ESCC patients who were primarily treated in Henan Cancer Hospital from 2010 to 2013 were collected for this study. Claudin-2 expression was analyzed by Immunohistochemistry and WB assay, and its relationship with clinicopathological characteristics and 5-year survival rate of ESCC patients was further investigated. The expression of Claudin-2 in ESCC cells (KYSE450, KYSE150, KYSE510 and KYSE140) and human immortalized esophageal epithelial SHEE cells was detected by WB assay. The Claudin-2 shRNA lentiviral vector was established and transfected into KYSE450 cells to establish a Claudin-2 knockdown cell line. Furthermore, the effects of knockdown of Claudin-2 on the proliferation, migration and invasion of KYSE450 cells were tested by clone formation experiment, cell scratch experiment and Transwell experiment. Results: The positive rate of Claudin-2 in ESCC tissues was significantly higher than that in adjacent tissues (P<0.05). The expression of Claudin-2 in ESCC tissues was related to lymph node metastasis (P<0.05). The 5-year survival rate of Claudin-2 positive patients was significantly lower than that of negative patients (P<0.05). The KYSE450 cell line with Claudin-2 knockdown was successfully constructed. The number of clone formation, wound healing rate and number of invaded cells in the sh-Claudin-2 group were significantly lower than those in the sh-NT group and the control group (all P<0.05). Conclusion: The expression level of Claudin-2 in ESCC tissues is higher than that of the tumor-adjacent tissues, and is negatively related with 5-year survival rate of ESCC patients. Claudin-2 can promote the proliferation, migration and invasion of ESCC cells.
2021, 28(5):489-494.
DOI: 10.3872/j.issn.1007-385X.2021.05.010
Abstract:
[Abstract] Objective: To investigate the effect of miRNA-490-3p regulating Smad2/TGF-β on chemo-sensitivity of colorectal cancer to oxaliplatin. Methods: One hundred patients with colorectal cancer (CRC) who received oxaliplatin (OXA) chemotherapy after radical operation were selected as research subjects and divided into drug resistant group (n=40) and non-resistant group (n=60) according to the chemotherapy outcome. The level of miRNA-490-3p in peripheral blood of two groups of patients was detected by qPCR. Human CRC cell line SW480 and oxaliplatin resistant CRC cell line OXA-SW480 were selected for the study. The expression level of miRNA-490-3p in the two cell lines was detected by qPCR, and then the miRNA-490-3p over-expression vector was transfected into OXA-SW480 cells (over-expression group), in the meanwhile, the empty vector group (OXA-SW480 cells transfected with empty vector) and blank control group (OXA-SW480 cells without any treatment) were set up. CCK-8 was used to detect cell proliferation ability of each group, and different concentrations of OXA were used to treat cells of each group to calculate the half inhibitory concentration (IC50); Annexin Ⅴ-FITC/PI staining was used to detect cell apoptosis rate of each group; WB assay was used to detect the expression levels of Smad2 and TGF-β. Results: In CRC patients, the level of miR-490-3p in the peripheral blood of the drug-resistant group was significantly lower than that of the non-resistant group. In the CRC cells, the level of miR-490-3p in the OXA-SW480 cells was significantly lower than that of the normal SW480 cells (P<0.05). Compared with the empty vector group and the blank control group, the level of miR-490-3p in the over-expression group was significantly increased (all P<0.05), the proliferation inhibition rate and the apoptosis rate were significantly increased (all P<0.05), Smad2 protein level was significantly reduced (all P<0.05), and TGF-β protein level was significantly increased (all P<0.05). After OXA treatment, the IC50 of the over-expression group was significantly lower than that of the empty vector group and the blank control group (both P<0.05). According to the results of Pearson correlation analysis, the expression of miR-490-3p was negatively correlated with the expression of Smad2 (r=–0.943, P<0.01), but positively correlated with the expression of TGF-β (r=0.961, P<0.01). Conclusion: Over-expression of miRNA-490-3p can increase the OXA sensitivity of CRC SW480 cells, which is related to the Smad2/TGF-β signaling pathway.
[Abstract] Objective: To investigate the effect of miRNA-490-3p regulating Smad2/TGF-β on chemo-sensitivity of colorectal cancer to oxaliplatin. Methods: One hundred patients with colorectal cancer (CRC) who received oxaliplatin (OXA) chemotherapy after radical operation were selected as research subjects and divided into drug resistant group (n=40) and non-resistant group (n=60) according to the chemotherapy outcome. The level of miRNA-490-3p in peripheral blood of two groups of patients was detected by qPCR. Human CRC cell line SW480 and oxaliplatin resistant CRC cell line OXA-SW480 were selected for the study. The expression level of miRNA-490-3p in the two cell lines was detected by qPCR, and then the miRNA-490-3p over-expression vector was transfected into OXA-SW480 cells (over-expression group), in the meanwhile, the empty vector group (OXA-SW480 cells transfected with empty vector) and blank control group (OXA-SW480 cells without any treatment) were set up. CCK-8 was used to detect cell proliferation ability of each group, and different concentrations of OXA were used to treat cells of each group to calculate the half inhibitory concentration (IC50); Annexin Ⅴ-FITC/PI staining was used to detect cell apoptosis rate of each group; WB assay was used to detect the expression levels of Smad2 and TGF-β. Results: In CRC patients, the level of miR-490-3p in the peripheral blood of the drug-resistant group was significantly lower than that of the non-resistant group. In the CRC cells, the level of miR-490-3p in the OXA-SW480 cells was significantly lower than that of the normal SW480 cells (P<0.05). Compared with the empty vector group and the blank control group, the level of miR-490-3p in the over-expression group was significantly increased (all P<0.05), the proliferation inhibition rate and the apoptosis rate were significantly increased (all P<0.05), Smad2 protein level was significantly reduced (all P<0.05), and TGF-β protein level was significantly increased (all P<0.05). After OXA treatment, the IC50 of the over-expression group was significantly lower than that of the empty vector group and the blank control group (both P<0.05). According to the results of Pearson correlation analysis, the expression of miR-490-3p was negatively correlated with the expression of Smad2 (r=–0.943, P<0.01), but positively correlated with the expression of TGF-β (r=0.961, P<0.01). Conclusion: Over-expression of miRNA-490-3p can increase the OXA sensitivity of CRC SW480 cells, which is related to the Smad2/TGF-β signaling pathway.
2021, 28(5):495-503.
DOI: 10.3872/j.issn.1007-385X.2021.05.011
Abstract:
[Abstract] Objective: Analyze the expression, clinical significance and possible biological processes of minichromosome maintenance protein 3 (MCM3) in brain gliomas, and explore its relationship with glioma immunity. Methods: The databases GEPIA and Oncomine were searched online to obtain the expression of MCM3 in glioma tissues. The CGGA database was used to analyze the relationship between MCM3 expression and clinicopathological characteristics of gliomas online.At the same time, 24 tumor specimens of patients with glioma who underwent surgical treatment in the Department of Neurosurgery of Shanxi Provincial People's Hospital from January 2019 to March 2020 and 8 non-tumor control specimens were collected, and used immunohistochemical SP method to detect the expression of MCM3 to verify the bioinformatics analysis results. Kaplan-Meier survival curve was used to evaluate the effect of MCM3 on the prognosis of glioma in the TCGA and CGGA databases.The significant related genes of MCM3 were obtained through Linkedomic database, STRING database and Cytoscape software. Use the DAVID database to perform GO and KEGG analysis of MCM3 and its significant related genes to explore the biological processes they may participate in.Finally, explore the relationship between MCM3 expression and glioma immune infiltrating cells in the TIMER database. Results: Comprehensive bioinformatics analysis and clinical data verification showed that MCM3 was highly expressed in glioma tissues relative to normal tissues (P=0.024), and its expression level gradually increased with the pathological grade (P=0.001).Survival analysis showed that high expression of MCM3 was related to the poor prognosis of glioma (P<0.05).GO and KEGG analysis of MCM3 and its significant related genes showed that these genes are mainly enriched in cell cycle, DNA replication and regulation of DNA damage repair.TIMER database showed that in the glioma cohort, MCM3 was correlated with a variety of immune infiltrating cells (P<0.05). Conclusions: MCM3 is highly expressed in gliomas and is related to poor prognosis, which may be related to the cell cycle, DNA replication, regulation of DNA damage repair and immune microenvironment of glioma cells. MCM3 can promote the progression of glioma, and can be used as a prognostic indicator and potential therapeutic target for patients with glioma.
[Abstract] Objective: Analyze the expression, clinical significance and possible biological processes of minichromosome maintenance protein 3 (MCM3) in brain gliomas, and explore its relationship with glioma immunity. Methods: The databases GEPIA and Oncomine were searched online to obtain the expression of MCM3 in glioma tissues. The CGGA database was used to analyze the relationship between MCM3 expression and clinicopathological characteristics of gliomas online.At the same time, 24 tumor specimens of patients with glioma who underwent surgical treatment in the Department of Neurosurgery of Shanxi Provincial People's Hospital from January 2019 to March 2020 and 8 non-tumor control specimens were collected, and used immunohistochemical SP method to detect the expression of MCM3 to verify the bioinformatics analysis results. Kaplan-Meier survival curve was used to evaluate the effect of MCM3 on the prognosis of glioma in the TCGA and CGGA databases.The significant related genes of MCM3 were obtained through Linkedomic database, STRING database and Cytoscape software. Use the DAVID database to perform GO and KEGG analysis of MCM3 and its significant related genes to explore the biological processes they may participate in.Finally, explore the relationship between MCM3 expression and glioma immune infiltrating cells in the TIMER database. Results: Comprehensive bioinformatics analysis and clinical data verification showed that MCM3 was highly expressed in glioma tissues relative to normal tissues (P=0.024), and its expression level gradually increased with the pathological grade (P=0.001).Survival analysis showed that high expression of MCM3 was related to the poor prognosis of glioma (P<0.05).GO and KEGG analysis of MCM3 and its significant related genes showed that these genes are mainly enriched in cell cycle, DNA replication and regulation of DNA damage repair.TIMER database showed that in the glioma cohort, MCM3 was correlated with a variety of immune infiltrating cells (P<0.05). Conclusions: MCM3 is highly expressed in gliomas and is related to poor prognosis, which may be related to the cell cycle, DNA replication, regulation of DNA damage repair and immune microenvironment of glioma cells. MCM3 can promote the progression of glioma, and can be used as a prognostic indicator and potential therapeutic target for patients with glioma.
2021, 28(5):504-510.
DOI: 10.3872/j.issn.1007-385X.2021.05.012
Abstract:
Objective: To reveal the correlation between BRD (bromodomain)-containing protein family and hepatocellular carcinoma (HCC) from different perspectives such as transcripts, protein levels, gene mutations, protein interactions, corresponding signaling pathways and functional enrichment by searching and mining HCC-related data in multiple tumor public databases, and to explore the potential of BRDs as biological markers for tumor progression and prognosis prediction of HCC. Methods: The mRNA expression profile of all BRD-containing proteins and clinical information of HCC patients were obtained from UALCAN database, and their correlation was subsequently analyzed. The relationship between mRNA expression of BRDs and prognosis of HCC patients was analyzed by using TCGA database. The immunohistochemical results of BRDs in HCC tissues and normal liver tissues were obtained from The Human Protein Atlas, and the differential expression was compared. The STRING database was used to analyze the PPI (protein-protein interaction) network of BRDs, and the CYTOSCAPE software was used for the KEGG and GO analyses of the interacting molecules. Results: All the 7 BRD family members were highly expressed in HCC tissues (P<0.01) and were positively correlated with tumor grade and clinical stage in HCC patients (P<0.05); moreover, HCC patients with low BRD8 and BRD9 expression had better prognosis (P<0.01). In addition, BRD interacting proteins were mainly involved in histone acetylation modification and were highly enriched in HCC signaling pathways. The expressions of BRD1, BRD3, BRD4, BRD7, BRD8 and BRD9 in HCC patients with TP53 mutation were significantly higher than those in patients without TP53 mutation (P<0.05). Conclusion: The BRD-containing proteins might be used as potential biomarkers for tumor grade, clinical stage, and prognosis prediction of HCC patients.
Objective: To reveal the correlation between BRD (bromodomain)-containing protein family and hepatocellular carcinoma (HCC) from different perspectives such as transcripts, protein levels, gene mutations, protein interactions, corresponding signaling pathways and functional enrichment by searching and mining HCC-related data in multiple tumor public databases, and to explore the potential of BRDs as biological markers for tumor progression and prognosis prediction of HCC. Methods: The mRNA expression profile of all BRD-containing proteins and clinical information of HCC patients were obtained from UALCAN database, and their correlation was subsequently analyzed. The relationship between mRNA expression of BRDs and prognosis of HCC patients was analyzed by using TCGA database. The immunohistochemical results of BRDs in HCC tissues and normal liver tissues were obtained from The Human Protein Atlas, and the differential expression was compared. The STRING database was used to analyze the PPI (protein-protein interaction) network of BRDs, and the CYTOSCAPE software was used for the KEGG and GO analyses of the interacting molecules. Results: All the 7 BRD family members were highly expressed in HCC tissues (P<0.01) and were positively correlated with tumor grade and clinical stage in HCC patients (P<0.05); moreover, HCC patients with low BRD8 and BRD9 expression had better prognosis (P<0.01). In addition, BRD interacting proteins were mainly involved in histone acetylation modification and were highly enriched in HCC signaling pathways. The expressions of BRD1, BRD3, BRD4, BRD7, BRD8 and BRD9 in HCC patients with TP53 mutation were significantly higher than those in patients without TP53 mutation (P<0.05). Conclusion: The BRD-containing proteins might be used as potential biomarkers for tumor grade, clinical stage, and prognosis prediction of HCC patients.
2021, 28(5):511-517.
DOI: 10.3872/j.issn.1007-385X.2021.05.013
Abstract:
肿瘤细胞脂代谢在肿瘤发生过程中进行了重编程，与肿瘤发生发展、侵袭和转移等密切相关，是肿瘤演进过程中出现的一个普遍而又至关重要的代谢特征。同时，肿瘤微环境中免疫细胞亦发生了异常脂代谢，且肿瘤脂代谢重编程对免疫微环境中细胞的功能和状态也产生影响，进一步促进其恶性生物学行为。目前，通过对肿瘤异常脂代谢及其对肿瘤免疫的影响的广泛探究，在发现肿瘤代谢特征和其影响肿瘤生物学行为的分子机制，以及肿瘤演进过程中代谢的适应性和复杂性等方面取得了众多的新突破。靶向肿瘤和免疫脂代谢相关基因与酶的研究已为肿瘤防治提供了有力的证据、开辟了新的思路，并为抗肿瘤治疗策略带来变革，有望在直接靶向肿瘤的同时靶向免疫细胞脂代谢以激活抗肿瘤免疫反应，实现“双管齐下”的治疗模式。本文综述了肿瘤细胞和免疫细胞的不同脂代谢特征以及不同脂质代谢对肿瘤演进和免疫细胞功能的重要影响，并概述了针对肿瘤免疫脂代谢异常的抗肿瘤治疗策略。
肿瘤细胞脂代谢在肿瘤发生过程中进行了重编程，与肿瘤发生发展、侵袭和转移等密切相关，是肿瘤演进过程中出现的一个普遍而又至关重要的代谢特征。同时，肿瘤微环境中免疫细胞亦发生了异常脂代谢，且肿瘤脂代谢重编程对免疫微环境中细胞的功能和状态也产生影响，进一步促进其恶性生物学行为。目前，通过对肿瘤异常脂代谢及其对肿瘤免疫的影响的广泛探究，在发现肿瘤代谢特征和其影响肿瘤生物学行为的分子机制，以及肿瘤演进过程中代谢的适应性和复杂性等方面取得了众多的新突破。靶向肿瘤和免疫脂代谢相关基因与酶的研究已为肿瘤防治提供了有力的证据、开辟了新的思路，并为抗肿瘤治疗策略带来变革，有望在直接靶向肿瘤的同时靶向免疫细胞脂代谢以激活抗肿瘤免疫反应，实现“双管齐下”的治疗模式。本文综述了肿瘤细胞和免疫细胞的不同脂代谢特征以及不同脂质代谢对肿瘤演进和免疫细胞功能的重要影响，并概述了针对肿瘤免疫脂代谢异常的抗肿瘤治疗策略。
2021, 28(5):518-525.
DOI: 10.3872/j.issn.1007-385X.2021.05.014
Abstract:
肿瘤免疫治疗是一种通过增强自身免疫应答来治疗肿瘤的新兴策略，能够防止肿瘤的转移和复发。然而，由于肿瘤的复杂性、患者的异质性及肿瘤免疫抑制微环境等问题的存在，导致免疫治疗整体有效率仅20%左右。近年来，纳米材料以其良好的生物相容性、靶向性和可控释放等优势，在肿瘤免疫治疗领域受到了越来越广泛的关注。纳米材料能够赋予免疫刺激分子、治疗药物等靶向肿瘤的能力，增强肿瘤部位药物的聚集，达到局部免疫调节，改善免疫抑制微环境，提高肿瘤免疫治疗的效果。本文就目前免疫治疗的现状及多种纳米材料在提高免疫治疗效果中的研究进展进行综述。
肿瘤免疫治疗是一种通过增强自身免疫应答来治疗肿瘤的新兴策略，能够防止肿瘤的转移和复发。然而，由于肿瘤的复杂性、患者的异质性及肿瘤免疫抑制微环境等问题的存在，导致免疫治疗整体有效率仅20%左右。近年来，纳米材料以其良好的生物相容性、靶向性和可控释放等优势，在肿瘤免疫治疗领域受到了越来越广泛的关注。纳米材料能够赋予免疫刺激分子、治疗药物等靶向肿瘤的能力，增强肿瘤部位药物的聚集，达到局部免疫调节，改善免疫抑制微环境，提高肿瘤免疫治疗的效果。本文就目前免疫治疗的现状及多种纳米材料在提高免疫治疗效果中的研究进展进行综述。
2021, 28(5):526-530.
DOI: 10.3872/j.issn.1007-385X.2021.05.015
Abstract:
白介素-33（IL-33）是一种双功能的细胞因子，也称为核因子，属于IL-1家族成员。在机体稳态下，IL-33主要在上皮细胞、内皮细胞和成纤维细胞中表达。当组织损伤、感染或坏死时，细胞分泌IL-33，发挥“危险信号”蛋白作用。IL-33特异性受体ST2在多种免疫细胞中表达，可引起广泛的免疫反应。研究IL-33在变态反应、感染、炎症，尤其在肿瘤发生发展过程中的作用具有重要意义。本文就IL-33对免疫细胞的影响及其作用机制的研究进展作一综述。
白介素-33（IL-33）是一种双功能的细胞因子，也称为核因子，属于IL-1家族成员。在机体稳态下，IL-33主要在上皮细胞、内皮细胞和成纤维细胞中表达。当组织损伤、感染或坏死时，细胞分泌IL-33，发挥“危险信号”蛋白作用。IL-33特异性受体ST2在多种免疫细胞中表达，可引起广泛的免疫反应。研究IL-33在变态反应、感染、炎症，尤其在肿瘤发生发展过程中的作用具有重要意义。本文就IL-33对免疫细胞的影响及其作用机制的研究进展作一综述。
2021, 28(5):531-536.
DOI: 10.3872/j.issn.1007-385X.2021.05.016
Abstract:
AXL是受体酪氨酸激酶TAM（TYRO3-AXL-MERTK）家族中的一员，被认为是一种癌基因，不仅在多种癌症中高表达，而且也表达于包括NK细胞、树突状细胞（DC）、T细胞在内的多种免疫细胞，且可以通过调节其下游的信号通路影响免疫细胞的发育及功能。AXL作为一种“免疫检查点”参与抗肿瘤免疫反应的调控，或将成为肿瘤免疫治疗的新靶点。本文主要介绍AXL在不同免疫细胞中的生物学功能，以及目前靶向AXL相关药物的研究进展，以期为研发AXL靶向药物和制定联合用药策略提供新思路。
AXL是受体酪氨酸激酶TAM（TYRO3-AXL-MERTK）家族中的一员，被认为是一种癌基因，不仅在多种癌症中高表达，而且也表达于包括NK细胞、树突状细胞（DC）、T细胞在内的多种免疫细胞，且可以通过调节其下游的信号通路影响免疫细胞的发育及功能。AXL作为一种“免疫检查点”参与抗肿瘤免疫反应的调控，或将成为肿瘤免疫治疗的新靶点。本文主要介绍AXL在不同免疫细胞中的生物学功能，以及目前靶向AXL相关药物的研究进展，以期为研发AXL靶向药物和制定联合用药策略提供新思路。
2021, 28(5):537-544.
DOI: 10.3872/j.issn.1007-385X.2021.05.017
Abstract:
硫化氢（H2S）是近年来在哺乳动物体内发现的第三种气体信号分子。H2S通过多种信号转导途径在人体的多个生理系统以及肿瘤的发生发展中发挥重要的调节作用。本文对于H2S的生物学特点、内源性与外源性H2S的产生途径及其在结直肠癌发生发展中的作用作一综述，并详细探讨H2S的抑制剂、H2S供体、H2S与化疗药物或新型纳米材料联合在结直肠癌精准治疗方面的最新研究进展。针对H2S及其相关信号通路的药物前体或治疗策略在结直肠癌的治疗研究中已展现出巨大的潜力，有必要引起更广泛的关注。
硫化氢（H2S）是近年来在哺乳动物体内发现的第三种气体信号分子。H2S通过多种信号转导途径在人体的多个生理系统以及肿瘤的发生发展中发挥重要的调节作用。本文对于H2S的生物学特点、内源性与外源性H2S的产生途径及其在结直肠癌发生发展中的作用作一综述，并详细探讨H2S的抑制剂、H2S供体、H2S与化疗药物或新型纳米材料联合在结直肠癌精准治疗方面的最新研究进展。针对H2S及其相关信号通路的药物前体或治疗策略在结直肠癌的治疗研究中已展现出巨大的潜力，有必要引起更广泛的关注。
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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.