MiR-192-5p regulates the proliferation and apoptosis of cholangiocarcinoma cells by activating MEK/ERK pathway
- 3 Biotech. 2021 Feb;11(2):99. doi: 10.1007/s13205-021-02650-w.
- 1. Department of Hepatobiliary Surgery, General Hospital of Ningxia Medical University, No. 804 Shengli South Street, Xingqing District, Yinchuan, 750001 Ningxia Province China.
- 2. Department of Special Ward of Surgery, Shanxi Cancer Hospital, Taiyuan, 030013 Shanxi Province China.
- 3. Department of General Surgery, the First Affiliated Hospital of Xi 'an Medical College, Xi 'an, 710077 Shanxi Province China.
- # Contributed equally.
Objective: Cholangiocarcinoma (CCA) is the second most common liver Cancer, characterized by late diagnosis and fatal outcome. Although miR-192-5p has been shown to have a vital role in various cancers, its role in CCA is unknown. Here, we investigated the role of miR-192-5p in CCA cell proliferation and Apoptosis, and elucidated its potential mechanism of action.
Methods: The miR-192-5p expression in CCA tissues and cell lines was detected by real-time quantitative reverse transcription-polymerase chain reaction. Cell proliferation was analyzed using the cell counting Kit-8 and 5-bromodeoxyuridine staining assays, while Apoptosis was examined by flow cytometry and the terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling assay. Western blot analysis was used to measure the expression of cell proliferation and apoptosis-related proteins, as well as MEK/ERK signaling pathway-related proteins.
Results: MiR-192-5p was highly expressed in CCA tissues and cell lines. Overexpression of miR-192-5p significantly promoted CCA proliferation, and inhibited Apoptosis. The MEK Inhibitor, PD98059, reversed these miR-192-5p-induced effects on MEK/ERK signaling-associated protein expression, proliferation promotion, and Apoptosis inhibition in TFK-1 cells.
Conclusion: MiR-192-5p promotes proliferation and suppressed Apoptosis of CCA cells via the MEK/ERK pathway, which may be a potential therapeutic strategy for CCA treatment.