Effect of miR-375 on non-small cell lung carcinoma invasion, migration, and proliferation through the CIP2A pathway

Author:

Wu Junyu1,Yuan Weijun2,Wang Yuhuan2,Zhao Xiaodong1

Affiliation:

1. Department of Emergency, The Fourth Medical Center of General Hospital of Chinese People's Liberation Army, Beijing 100037, China

2. Department of Special Medicine, School of Basic Medical College, Qingdao University, Qingdao 266021, China

Abstract

Abstract Objective The aim of this study was to study the effect of miR-375 on non-small cell lung carcinoma (NSCLC) invasion, migration, and proliferation through the CIP2A pathway. Methods We constructed a stable over-expressing cell line with lentivirus as the experimental group (Lv-miR-375) and transfected the empty vector as the negative control group (Lv-NC). The expression level of miR-375 was detected using real-time fluorescence quantitative PCR (qRT-PCR).Western blots were used to detect the expression levels of cancerous inhibitor of PP2A (CIP2A), MYC, protein kinase B (AKT) and p-AKT in Lv-NC- and Lv-miR-375-transfected cells. Transwell assays were conducted to detect the cell invasion and metastasis ability, and the cell counting kit-8 (CCK8) was used to detect cell proliferation. Results qRT-PCR showed that miR-375 was overexpressed in NSCLC. Compared to the Lv-NC-transfected cells, the western blot results showed that CIP2A, MYC and p-AKT were highly expressed in Lv-miR-375-transfected cells. Transwell assays showed that the invasion and migration ability of Lv-miR-375-transfected A549 cells was significantly higher than that of Lv-NC-transfected cells. CCK8 experiments showed that compared to Lv-NC-transfected cells, the cell proliferation ability of the Lv-miR-375-transfected cells increased. Conclusion MiR-375 could promote the invasion, migration, and proliferation of NSCLC A549 cells via the CIP2A pathway. MiR-375 is expected to become a new target for the treatment of NSCLC, and may become an important biomarker for the diagnosis, prognosis, and treatment of the disease.

Publisher

Ovid Technologies (Wolters Kluwer Health)

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