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Expression of miR-195 and MEK1 in patients with bladder cancer and their relationship to prognosis
Kun Yang1, Hai Tang1, Mantang Ding1
1Department of Urology, Jing'an District Centre Hospital of Shanghai (Huashan Hospital Fudan University Jing'an Branch) Shanghai, China.
Objective:
MAPK kinase 1 (MEK1) plays an important role in regulating cell proliferation and apoptosis through activation of the ERK/MAPK signaling pathway. It was found that the expression of miR-195 in bladder cancer was abnormally decreased, suggesting that miR-195 may affect the development of bladder cancer. In this study, we examined the expression of miR-195 and MEK1 in bladder cancer tissues and analyzed the relationship between miR-195 and MEK1 in cell proliferation and apoptosis in bladder cancer cells.
Patients And Methods:
The expression of MEK1 in bladder cancer tissues was detected by western blot, and the expression levels of miR-195 and MEK1 mRNA were detected by qRT-PCR. Log Rank test was used to compare the survival and prognosis of patients with low and high expression of miR-195 and MEK1 by using the median expression of miR-195 and MEK1. Bioinformatics analysis and double luciferase reporter gene test were used to verify the relationship between miR-195 and MEK1. Bladder cancer BIU-87 and 5637 cells were cultured in vitro and divided into two groups: miR-NC group and miR-195 mimic group. The expression of MEK1 and p-MEK1 protein was detected by western blot, apoptosis was detected by flow cytometry, and cell proliferation was detected by EdU staining.
Results:
Compared with normal bladder tissue, expression of miR-195 in bladder cancer tissue was significantly decreased, while the expression of MEK1 mRNA and protein was significantly increased. The prognosis of patients with low expression of miR-195 was worse than those with high expression of miR-195. The prognosis of patients with low expression of MEK1 was better than those with high expression of MEK1. Bioinformatics analysis showed that there was a target complementary binding site between miR-195 and MEK1. Double luciferase reporter gene experiments confirmed that there was a target regulatory relationship between miR-195 and MEK1. miR-195 mimic transfection could significantly down-regulate the expression of MEK1 and p-MEK1 proteins in BIU-87 and 5637 cells, weaken cell proliferation, and increase cell apoptosis.
Conclusion:
Overexpression of miR-195 can inhibit the proliferation of bladder cancer cells by inhibiting MEK1, which provides further evidence for developing therapy against bladder cancer.
