Mobile website
Archive > Volume 25 Issue 10 > 2018,25(10):994-998. DOI:10.3872/j.issn.1007-385X.2018.10.004 Prev Next
Basic Research
VPApromotesEMTin colon carcinoma cells via nuclear translocation of E-cadherin
- Article
- Figures
- Metrics
- Preview PDF
- Reference
- Related
- Cited by
- Materials
Abstract:
Objective: To explore the effect of histone deacetylase (HDAC) inhibitor valproic acid (VPA) on the epithelial-mesenchymal transition (EMT) of colon cancer. Methods: With four colon carcinoma cell lines (DLD-1, HCT116, SW480 and HT29) as study subjects, the effect of different concentrations of VPA (0.5，5 mmol/L) on cell proliferation was detected by MTT assay. The expression level of EMT-related proteins (E-cadherin and vimentin) was detected by Western blotting; Phenotypic changes of E-cadherin and vimentin were detected by immunofluorescence staining; Cell migration and invasion ability was detected by wound healing and Transwell invasion assay, respectively. Results: After treated with different concentrations of VPA for 48 h, low concentration of VPA merely exerted any effect on the cell proliferation rate of four colon cancer cell lines, and thus was chosen as the experiment concentration;The results of Western blotting showed that the expression of E-cadherin was reduced (P<0.05) and vimentin was increased (P<0.05) in colon carcinoma cells by VPA treatment (0.5 mmol/L); Immunofluorescence staining revealed membranous attenuation or nuclear translocation of E-cadherin and enhanced expression of vimentin after VPA treatment (0.5 mmol/L), and these responses occurred after 6 h and sustained until 24 h; Wound healing and Transwell invasion assay showed increased migration and invasion ability following VPA treatment (0.5 mmol/L). Conclusion: Low concentration VPA could induce the development of EMT in colon cancer cells by nuclear translocation of E-cadherin, and obviously enhance the migration and invasion ability of colon cancer cells; Thus, HDAC inhibitors, as a new type anti-cancer option, shall be carefully considered before their application in colon cancer.
Keywords:
Project Supported:
Project supported by the National Natural Science Foundation of China（No.413010173）
Clc Number:
