scholarly journals miR-200c /FUT4 axis prevents the migration, invasion and proliferation of colon cancer cells by downregulating Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Negative Control ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Ki 67 ◽  
Sw480 Cells ◽  
Related Proteins

Abstract Background To investigate the effects of miR-200c targeting fucosyltransferase 4 (FUT4) on the proliferation, migration and invasion of colon cancer cells and further to explore its mechanism. Methods The expression of miR-200c and FUT4 mRNA in Lovo and SW480 cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and their correlation was analyzed by Pearson. LipofectamineTM 2000 transfection reagent was used to transfect miR-200c mimic, FUT4 siRNA, FUT4 mimic and FUT4 mimic negative control into Lovo and SW480 cells, and RT-PCR was used to analyze the effect of transfection. Cell counting kitcck-8 (CCK-8), cloning and transwell assays were used to detect the migration, invasion and proliferation of Lovo and SW480 cells, respectively. Immunofluorescence was used to analyze the expression of Ki-67 protein. Moreover, the expression of Wnt/β-catenin signaling pathway-related proteins were detected by western blot. Double luciferase experiment was performed to verify the targeting relationship between miR-200c and FUT4. Results Pearson results showed that miR-200c and FUT4 were negatively correlated in Lovo and SW480 cells (correlation coefficients were − 0.9046 and − 0.9236, respectively). MiR-200c overexpression inhibits the proliferation, migration and invasion of Lovo cells by down-regulating FUT4. The expression of Ki67 positive cells and Wnt/β-catenin signaling pathway-related proteins were reduced in miR-200c overexpression and FUT4 silencing groups. The scientific search and dual luciferase reporting system identified FUT4 was the target of miR-200c. Conclusion In conclusion, miR-200c overexpression inhibits FUT4 expression and down-regulates the Wnt/β-catenin signaling pathway, thereby inhibiting the migration, invasion and proliferation of colon cancer cells.

scholarly journals The miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Correlation Analysis ◽  
Cancer Cells ◽  
Pearson Correlation ◽  
Signalling Pathway ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Pearson Correlation Analysis ◽  
Sw480 Cells ◽  
Related Proteins

Abstract BackgroundTo investigate the effects of miR-200c, which targets fucosyltransferase 4 (FUT4), on the proliferation, migration and invasion of colon cancer cells and to further explore its mechanism.MethodsWe assessed the miR-200c and FUT4 mRNA levels in LoVo and SW480 cells by quantitative real-time polymerase chain reaction (qRT-PCR), and their correlation was analysed by Pearson correlation analysis. LipofectamineTM 2000 transfection reagent was used to transfect miR-200c mimic, FUT4 siRNA, FUT4 mimic and FUT4 mimic negative control into LoVo and SW480 cells, and RT-PCR was used to analyse the transfection efficiency. Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were used to detect the migration, invasion and proliferation of LoVo and SW480 cells. Immunofluorescence was used to analyse the expression of the Ki-67 protein. Moreover, the expression of Wnt/β-catenin signalling pathway-related proteins was detected by western blots. A double luciferase experiment was performed to verify the targeting relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin signalling pathway-related proteins were also analysed. ResultsPearson correlation analysis showed that miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A bioinformatics analysis and a dual luciferase reporting system identified FUT4 as the target of miR-200c. ConclusionsIn conclusion, miR-200c overexpression inhibits FUT4 expression and downregulates the Wnt/β-catenin signalling pathway, thereby inhibiting the migration, invasion and proliferation of colon cancer cells.

scholarly journals Epithelial–mesenchymal transition and metastasis of colon cancer cells induced by the FAK pathway in cancer-associated fibroblasts

2020 ◽  
Vol 48 (6) ◽  
pp. 030006052093124
Author(s):  
Xuefeng Xuefeng ◽  
Ming-Xing Hou ◽  
Zhi-Wen Yang ◽  
Agudamu Agudamu ◽  
Feng Wang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
3D Culture ◽  
Cancer Associated Fibroblasts ◽  
Colon Cancer Cells ◽  
Mesenchymal Transition ◽  
Lovo Cells ◽  
Related Proteins

Objective The role and mechanism of tetrathiomolybdate (TM) in cancer-associated fibroblasts (CAFs) in colon cancer using three-dimensional (3D) culture were investigated, and the associations between the focal adhesion kinase (FAK) pathway and epithelial–mesenchymal transition (EMT) in CAFs were explored. Methods A 3D co-culture model of colon cancer LOVO cells with CAFs and normal fibroblasts (NFs) was established using Matrigel as a scaffold material. The differential expression of LOXL2 (lysyl oxidase-like 2) in the supernatant of CAFs and NFs was determined using ELISA, and expression levels of EMT-related proteins and FAK signaling pathway-related proteins were determined using western blot. Results LOXL2 levels secreted by CAFs were higher compared with that secreted by NFs. In the CAF + LOVO group, compared with the LOVO group, E-cadherin expression decreased significantly, while N-cadherin and F-PAK expression increased significantly. TM results were opposite compared with the above results. Conclusions CAFs stimulate EMT in human colon cancer LOVO cells by secreting LOXL2 to activate the FAK signaling pathway, thereby promoting tumor metastasis. TM inhibited the occurrence of EMT in the CAF-induced colon cancer LOVO cell line, thereby reducing the invasion and metastasis of colon cancer cells.

scholarly journals The significance of homeodomain transcription factor 2 in colon cancer cells

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yang He ◽  
Peng Gong ◽  
Sitong Wang ◽  
Qing Xu ◽  
Jianhua Chen
Keyword(s):  
Cervical Cancer ◽  
Colon Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Homeodomain Transcription Factor ◽  
Non Coding Rna ◽  
Related Proteins ◽  
Long Non Coding Rna

Abstract Background Colon cancer is a serious malignant tumor. It has been reported that paired-like homeodomain transcription factor 2 (PITX2) can promote the progression of several types of cancer via regulating the Wnt/β-catenin pathway. It has also been demonstrated that high levels of long non-coding RNA (lncRNA) gastric carcinoma high expressed transcript 1 (GHET1) can also promote the development of cervical cancer via activating the Wnt/β-catenin pathway. However, whether PITX2 can affect the development of colon cancer via regulating the expression of lncRNA GHET1 remains unclear. Results The results demonstrated that PITX2 knockdown attenuated the proliferation, migration and invasion abilities of colon cancer cells. Additionally, PITX2 promoted the expression of lncRNA GHET1 via binding to its promoter. Overexpression of lncRNA GHET1 induced the expression of Wnt/β-catenin signaling-related proteins, cyclin D1, c-Myc and MMP-7. Furthermore, lncRNA GHET1 overexpression abrogated the PITX2 silencing-mediated decreased proliferation, migration and invasion abilities of colon cancer cells. Conclusion The findings of the present study suggested that PITX2 could enhance the proliferation, migration and invasion abilities of colon cancer cells via upregulating lncRNA GHET1 and activating the Wnt/β-catenin pathway.

scholarly journals Tumor Suppressive Role of ARHGAP17 in Colon Cancer Through Wnt/β-Catenin Signaling

2018 ◽  
Vol 46 (5) ◽  
pp. 2138-2148 ◽  
Author(s):  
Shengli Pan ◽  
Yingying Deng ◽  
Jun Fu ◽  
Yuhao Zhang ◽  
Zhijin Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Wnt Signaling ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Rho Gtpase ◽  
Gene Set Enrichment Analysis ◽  
Cell Counting ◽  
Normal Colonic Mucosa ◽  
Colon Cancer Cells

Background/Aims: A few Rho GTPase activating proteins (RhoGAPs) have been identified as tumor suppressors in a variety of human cancers. ARHGAP17, a member of RhoGAPs, has been reported to be involved in the maintenance of tight junction and epithelial barrier. The present study aimed to explore its expression in colon cancer and the possible function in colonic carcinogenesis. Methods: The mRNA and protein expression was assessed by realtime PCR and immunoblotting, respectively. Cell Counting Kit-8 (CCK-8) and Transwell assays were performed to evaluate cell proliferation and invasion, respectively. Results: We found that ARHGAP17 expression was obviously lower in colon cancer specimens than in normal colonic mucosa. ARHGAP17 expression was associated with tumor stage, size and differentiation. In vitro analysis demonstrated that ARHGAP17 overexpression inhibited cell growth and invasion of HCT-8 and HCT-116 cells. In addition, an in vivo experimental metastasis model showed that ARHGAP17 overexpression restricted cancer metastasis to the lung. Mechanically, we found that Wnt signaling contributed to the functions of ARHGAP17 in colon cancer cells. Gene set enrichment analysis (GSEA) in The Cancer Genome Atlas dataset showed that the Wnt signaling pathway was negatively associated with ARHGAP17 expression. The mRNA expression of β-catenin (an important signaling transducer of canonical Wnt signaling) gene (CTNNB1) was negatively correlated with ARHGAP17 expression. Immunoblot analysis of downstream effectors of β-catenin (c-Myc/p27 and MMP7) in ARHGAP17 overexpressing colon cancer cells and metastatic tumors within the lung also validated the GSEA result. ARHGAP17 overexpression increased the phosphorylation of glycogen synthetase kinase 3β, and decreased β-catenin nuclear localization and transcriptional activity. Furthermore, inhibition of Wnt signaling by Wnt Inhibitor Factor-1 (WIF-1) in HIEC cells with ARHGAP17 knockdown significantly attenuated the promotion effects of ARHGAP17 knockdown on cell proliferation, invasion and the activation of β-catenin. Conclusion: these results suggest that ARHGAP17 might serve as a tumor suppressor in colon cancer progression and metastasis through Wnt/β-catenin signaling pathway.

scholarly journals miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Biological Behaviour ◽  
Western Blots ◽  
Sw480 Cells ◽  
Related Proteins

Abstract BackgroundMicroRNA(miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer.MethodsThe miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed. ResultsIn vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study.ConclusionsIn summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.

scholarly journals Activation of P2×7 Receptor Promotes the Invasion and Migration of Colon Cancer Cells via the STAT3 Signaling

2020 ◽  
Vol 8 ◽  
Author(s):  
Wen-jun Zhang ◽  
Ce-gui Hu ◽  
Hong-liang Luo ◽  
Zheng-ming Zhu
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Receptor Activation ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Stat3 Pathway ◽  
Invasion And Migration ◽  
Sw480 Cells ◽  
And Migration

The pathological mechanism of colon cancer is very complicated. Therefore, exploring the molecular basis of the pathogenesis of colon cancer and finding a new therapeutic target has become an urgent problem to be solved in the treatment of colon cancer. ATP plays an important role in regulating the progression of tumor cells. P2 × 7 belongs to ATP ion channel receptor, which is involved in the progression of tumors. In this study, we explored the effect and molecular mechanism of ATP-mediated P2 × 7 receptor on the migration and metastasis of colon cancer cells. The results showed that ATP and BzATP significantly increased the inward current and intracellular calcium concentration of LOVO and SW480 cells, while the use of antagonists (A438079 and AZD9056) could reverse the above phenomenon. We found that ATP promoted the migration and invasion of LOVO and SW480 cells and is dose-dependent on ATP concentration (100–300 μM). Similarly, BzATP (10, 50, and 100 μM) also significantly promoted the migration and invasion of colon cancer cells in a concentration-dependent manner. While P2 × 7 receptor antagonists [A438079 (10 μM), AZD9056 (10 μM)] or P2 × 7 siRNA could significantly inhibit ATP-induced colon cancer cell migration and invasion. Moreover, in vivo experiments showed that ATP-induced activation of P2 × 7 receptor promoted the growth of tumors. Furthermore, P2 × 7 receptor activation down-regulated E-cadherin protein expression and up-regulated MMP-2 mRNA and concentration levels. Knocking down the expression of P2 × 7 receptor could significantly inhibit the increase in the expression of N-cadherin, Vimentin, Zeb1, and Snail induced by ATP. In addition, ATP time-dependently induced the activation of STAT3 via the P2 × 7 receptor, and the STAT3 pathway was required for the ATP-mediated invasion and migration. Our conclusion is that ATP-induced P2 × 7 receptor activation promotes the migration and invasion of colon cancer cells, possibly via the activation of STAT3 pathway. Therefore, the P2 × 7 receptor may be a potential target for the treatment of colon cancer.

scholarly journals Long Non-Coding RNA ELFN1-AS1 Promoted Colon Cancer Cell Growth and Migration via the miR-191-5p/Special AT-Rich Sequence-Binding Protein 1 Axis

2021 ◽  
Vol 10 ◽  
Author(s):  
Yongjun Du ◽  
Yanmei Hou ◽  
Yongbo Shi ◽  
Juan Liu ◽  
Tingxin Li
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Early Stage ◽  
Binding Protein ◽  
Colon Adenocarcinoma ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Cell Growth And Migration

Long non-coding RNAs (lncRNAs) are reported to participate in tumor development. It has been manifested in previous researches that lncRNA ELFN1-AS1 is involved in early-stage colon adenocarcinoma with potential diagnostic value. However, no studies have revealed the specific mechanism of ELFN1-AS1 in colon cancer, and there are no other studies on whether ELFN1-AS1 is associated with tumorigenesis. In our study, ELFN1-AS1 with high expression in colon cancer was selected by TCGA analysis, and the survival analysis was carried out to verify it. Subsequently, qRT-PCR was adopted for validating the results in tissues and cell lines. Cell counting kit-8 (CCK8), 5-ethynyl-2’-deoxyuridine (EdU), cell colon, cell apoptosis, cell cycle, cell migration, and invasion assays were utilized to assess the role of ELFN1-AS1 in colon cancer. Results uncovered that ELFN1-AS1 expression was prominently raised in colon cancer cells and tissues. ELFN1-AS1 decrement restrained cells to grow through interfering with distribution of cell cycle and promoting apoptosis. Meanwhile, ELFN1-AS1 decrement weakened the capacity of cells to migrate and invade. What’s more, ELFN1-AS1 was uncovered to act as a competing endogenous RNA (ceRNA) to decrease miR-191-5p expression, thus raising special AT-rich sequence-binding protein 1 (SATB1), a downstream target of ceRNA. To sum up, ELFN1-AS1 drives colon cancer cells to proliferate and invade through adjusting the miR-191-5p/SATB1 axis. The above results disclose that lncRNA ELFN1-AS1 is possibly a novel treatment target for colon cancer cases.

scholarly journals MiR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jinchun Cong ◽  
Jian Gong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Biological Behaviour ◽  
Western Blots ◽  
Sw480 Cells ◽  
Related Proteins

Abstract Background MicroRNA (miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer. Methods The miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed. Results In vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were − 0.9046 and − 0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study. Conclusions In summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.

scholarly journals The miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Biological Behaviour ◽  
Western Blots ◽  
Sw480 Cells ◽  
Related Proteins

Abstract BackgroundMicroRNA(miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer.MethodsThe miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed.ResultsIn vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study.ConclusionsIn summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.

scholarly journals INHBA promotes the proliferation, migration and invasion of colon cancer cells through the upregulation of VCAN

2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110149
Author(s):  
Jia Guo ◽  
Yuan Liu
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Counting ◽  
Migration And Invasion ◽  
High Morbidity ◽  
Colon Cancer Cells ◽  
Invasion And Migration ◽  
And Migration ◽  
Cancer Tissues

Objective Colon cancer has high morbidity and mortality rates, and proliferation, invasion and migration play an important role in colon cancer progression. Here, the effects of inhibin subunit beta A (INHBA) on cell proliferation, invasion and migration were investigated. Methods The UALCAN database was used to assess INHBA expression in colon cancer tissues and predict the survival of patients with high and low INHBA expression. The relevant proteins were detected by RT-qPCR and western blot. Cell transfection was performed to overexpress or inhibit INHBA and versican (VCAN). The high correlation between INHBA and VCAN found through LinkedOmics and StarBase databases was verified by immunoprecipitation assays. Cell proliferation was detected by cell counting kit-8 and colony formation assays. Wound healing and Transwell assays were used to assess migration and invasion. Results INHBA expression was upregulated in colon cancer tissues and cells. INHBA inhibition impaired the proliferation, migration and invasion of these cells. In addition, we confirmed the correlation between INHBA and VCAN in colon cancer cells. Finally, we found that INHBA interference inhibited the aggressive behavior of colon cancer cells by downregulating VCAN. Conclusion INHBA promotes the proliferation, migration and invasion of colon cancer cells through the upregulation of VCAN.

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