MACC1 silencing inhibits cell proliferation and induces cell apoptosis of lung adenocarcinoma cells through the β-catenin pathway
| Autor: | Song-Lei Ou, Suli Zhang, Lin Guo, Y Lai, Xu-chen Ma |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Cancer Research Lung Neoplasms Adenocarcinoma of Lung Apoptosis Flow cytometry 03 medical and health sciences 0302 clinical medicine Cyclin D1 Carcinoma Non-Small-Cell Lung Cell Line Tumor medicine Humans Gene Silencing beta Catenin Cell Proliferation A549 cell Gene knockdown medicine.diagnostic_test Cell growth Chemistry Cell cycle medicine.disease Gene Expression Regulation Neoplastic 030104 developmental biology Oncology A549 Cells 030220 oncology & carcinogenesis Trans-Activators Cancer research Adenocarcinoma Transcription Factors |
| Zdroj: | Neoplasma. 65:552-560 |
| ISSN: | 1338-4317 |
| DOI: | 10.4149/neo_2018_170918n595 |
| Popis: | It has been documented that over-expression of metastasis-associated in colon cancer-1 (MACC1) is related to poor prognosis in non-small cell lung cancer (NSCLC). This study investigates the function and underlying molecular mechanisms of MACC1 in lung adenocarcinoma. Here, we firstly employed immunohistochemistry, western blotting, real-time PCR, and online database to demonstrate that MACC1 expression was elevated in tumor tissues compared with tumoradjacent or normal tissues. Real-time PCR, CCK-8, colony formation western blotting, Hoechst staining, and flow cytometry assays then evaluated the effects of MACC1 knockdown on the cell cycle, cell proliferation and apoptosis in A549 and H1299 adenocarcinoma cells. Result highlighted that MACC1 knockdown inhibited cell proliferation, induced G0/ G1 phase arrest and promoted cell apoptosis in vitro. Mechanistic analysis revealed it also up-regulated expression levels of bax, cleaved-caspase-3 and cleaved-PARP while down-regulating cyclin D1, c-myc, bcl-2, and β-catenin expression in A549 cells. Intriguingly, up-regulation of β-catenin suppressed G0/G1 phase arrest and apoptosis in MACC1-silenced A549 cells and this was accompanied by increased levels of cyclin D1, c-myc, and bcl-2. Collectively, our results indicate that MACC1 knockdown effectively inhibited cell proliferation and promoted apoptosis of lung adenocarcinoma cells by regulating the β-catenin pathway. |
| Databáze: | OpenAIRE |
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