<p>MiR-195-5p Inhibits Proliferation and Induces Apoptosis of Non-Small Cell Lung Cancer Cells by Targeting CEP55</p>

Abstract

Objective: This study aims to explore whether miR-195-5p can inhibit proliferation and induce apoptosis of non-small cell lung cancer (NSCLC) cells by targeting CEP55. Methods: qRT-PCR was used to measure the expression of miR-195-5p in NSCLC cells. MTT assay, colony formation assay, and flow cytometry were used to detect the role of miR-195-5p in NSCLC cells. Western blot was used to measure the protein expression of CEP55, Bax and Bcl-2 in cells. Dual-Luciferase assay was performed to verify the relationship between miR-195-5p and CEP55. Results: The expression of miR-195-5p was higher in human normal lung cell lines than in NSCLC cells. MiR-195-5p overexpression inhibited cell proliferation, which could block the cell cycle of A549 cell line in the G 0 /G 1 phase. Moreover, overexpression of miR-195-5p increased cell apoptotic rate of A549 cell lines, with the expression of pro-apoptotic protein Bax up-regulated and that of the anti-apoptotic protein Bcl-2 down-regulated. The Dual-Luciferase assay showed that miR-195-5p could specifically target CEP55. Furthermore, CEP55 was down-regulated in NSCLC cells. Overexpression of CEP55 enhanced the proliferation and colony formation ability of A549 cell line. Overexpression of CEP55 can reverse the inhibitory effect of miR-195-5p. Conclusion: MiR-195-5p inhibits proliferation and induces apoptosis of NSCLC cells by negatively regulating CEP55.

MiR-195-5p is a Potential Factor Responsible for CPNE1 Differential Expression between Subtypes of Non-Small Cell Lung Cancer

“…In ovarian cancer, overexpression of miR-195-5p can reduce cisplatin resistance and angiogenesis via PSAT1-depedent GSK3β/β-catenin signaling pathway [40]. To date, only four published papers have demonstrated the suppressive role of miR-195-5p in NSCLC cell proliferation and functioned as a predictor of poor prognosis [28][29][30][31]. In line with the published result, our further survival analysis proved that relatively low miR-195-5p expression was associated with unfavorable survival.…”

“…Moreover, miR-195-5p functions as a predictor of poor prognosis by directly targeting CIAPIN1 [30]. In addition, miR-195-5p Inhibited NSCLC cell proliferation and induced apoptosis by targeting CEP55 [31]. So we hypothesized whether miR-195-5p expression may be responsible for the differential expression among subtypes of lung cancer.…”

Circ_ZFR contributes to the paclitaxel resistance and progression of non-small cell lung cancer by upregulating KPNA4 through sponging miR-195-5p

“…For mechanism analysis, circ_ZFR was identified to serve as the sponge for miR-195-5p and then elevated KPNA4 expression. Luo et al declared that miR-195-5p upregulation restrained cell growth, cell cycle and facilitated apoptosis in NSCLC cells via binding to CEP55 [ 27 ]. Zheng et al demonstrated the tumor suppressive role of miR-195-5p in NSCLC by regulating CIAPIN1 [ 28 ].…”

Construction of a disease‐specific lncRNA‐miRNA‐mRNA regulatory network reveals potential regulatory axes and prognostic biomarkers for hepatocellular carcinoma

“…MiR-195 was reported to be downregulated in several cancers, and its overexpression could inhibit the proliferation and migration and regulate the G1/S transition of cancer cells in non-small cell lung cancer, breast cancer, and hepatocellular carcinoma. [52][53][54] In addition, miR-195-5p also acted as an anti-oncogene via targeting PHF19 in HCC. 54 CHEK1 was a serine/threonine-specific protein kinase mediating cell cycle arrest in response to DNA damage and functioned through the PLK-4/ATR/CHEK1 pathway in HCC.…”