MACC1 silencing inhibits cell proliferation and induces cell apoptosis of lung adenocarcinoma cells through the β-catenin pathway

• DOI: 10.4149/neo_2018_170918n595
• Publication Date: 2018-06-21T08:58:06Z
• Authors: L. GUO; S. OU; X. MA; S. ZHANG; Y. LAI
• Keywords: Lung Neoplasms; Adenocarcinoma of Lung; Apoptosis; 3. Good health; Gene Expression Regulation, Neoplastic; 03 medical and health sciences; 0302 clinical medicine; A549 Cells; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Trans-Activators; Humans; Gene Silencing; beta Catenin; Cell Proliferation; Transcription Factors

It has been documented that over-expression of metastasis-associated in colon cancer-1 (MACC1) is related to poor prognosis non-small cell lung cancer (NSCLC).This study investigates the function and underlying molecular mechanisms MACC1 adenocarcinoma.Here, we firstly employed immunohistochemistry, western blotting, real-time PCR, online database demonstrate expression was elevated tumor tissues compared with tumoradjacent or normal tissues.Real-time CCK-8, colony formation Hoechst staining, flow cytometry assays then evaluated effects knockdown on cycle, proliferation apoptosis A549 H1299 adenocarcinoma cells.Result highlighted inhibited proliferation, induced G0/ G1 phase arrest promoted vitro.Mechanistic analysis revealed it also up-regulated levels bax, cleaved-caspase-3 cleaved-PARP while down-regulating cyclin D1, c-myc, bcl-2, β-catenin cells.Intriguingly, up-regulation suppressed G0/G1 MACC1-silenced cells this accompanied by increased bcl-2.Collectively, our results indicate effectively regulating pathway.