AI Article Synopsis
- - The study investigates the role of miR-129-5p in gastric cancer, finding that its downregulation promotes epithelial-mesenchymal transition (EMT) and cell proliferation in cancer cells compared to normal cells.
- - Research methods included RT-qPCR, cell proliferation assays, western blot analysis, and luciferase assays, revealing that miR-129-5p directly targets and inhibits HMGB1, which is elevated in gastric cancer cells.
- - The findings suggest that increasing miR-129-5p levels could slow down cancer growth and EMT, highlighting its potential as a diagnostic and therapeutic target through the miR-129-5p/HMGB1 pathway.
Article Abstract
Background: The miR-129-5p has been reported to be aberrant expression and exert vital roles in tumor progression of various malignancies. However, the effects on EMT in gastric cancer and its precise molecular mechanism in gastric cancer remain unclear.
Methods And Materials: RT-qPCR was performed to evaluate the expression level of miR-129-5p and HMGB1 in cell lines. Cell proliferation was detected via CCK-8. The epithelial mesenchymal transition (EMT) related proteins and the expression of HMGB1 were detected by western blot analysis. Luciferase assays were used to validate binding seeds between miR-129-5p and HMGB1.
Results: miR-129-5p was downregulated in gastric cancer cells compared with GES-1. At the same time EMT was promoted in gastric cancer cells compared to GES-1. Overexpression of miR-129-5p inhibited EMT and proliferation. MiR-129-5p negatively and directly targeted HMGB1. HMGB1 was upregulated in gastric cancer cells and HMGB1 knocked-down inhibited EMT and cell proliferation.
Conclusion: Taken together, upregulation of miR-129-5p associated with gastric cancer proliferation and EMT, and serves as a potential diagnostic and therapeutic target via miR-129-5p/HMGB1 pathway in gastric cancer.
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| http://dx.doi.org/10.1016/j.prp.2018.12.024 | DOI Listing |
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