Open AccessDown-Regulation of 14-3-3σ Reduces Proliferation of Human Lung Cancers But Not Colon Cancer Cells
Author(s) -
Somrudee Nunun,
Paramee Thongsuksai,
Keson Trakunrum,
Pritsana Raungrut
Publication year - 2018
Publication title -
journal of health science and medical research (jhsmr)
Language(s) - English
Resource type - Journals
ISSN - 2586-9981
DOI - 10.31584/jhsmr.v36i2.3
Subject(s) - cell cycle , flow cytometry , cell growth , adenocarcinoma , cancer research , lung cancer , cell , colorectal cancer , a549 cell , cell cycle checkpoint , mtt assay , cancer , blot , g1 phase , chemistry , biology , microbiology and biotechnology , oncology , medicine , gene , biochemistry
Objective: 14-3-3σ protein is well known for its tumor suppressive function in breast cancer. However, recent evidence has raised the possibility that the 14-3-3σ protein may also have an oncogenic function in certain cancer types. The aim of this study was to investigate the oncogenic function of 14-3-3σ in adenocarcinoma cell lines of the lung (A549, H358) and colon (HT-29).Material and Methods: siRNA against 14-3-3σ was used to suppress 14-3-3σ expression. Cell proliferation, cell-cycle distribution and expression of related molecules were determined by MTT, flow cytometry, and western blotting, respectively.Results: Down-regulation of 14-3-3σ significantly reduced the proliferation of A549 and H358 by 35.0% and 31.0%, respectively, and significantly induced cell cycle arrest at the G0/G1 and G2/M phases, respectively. Increased p21 expression by 43.0% was only observed in si-14-3-3σ-H358 cells. The si-14-3-3σ-HT-29 cells showed no alteration of cell proliferation and cell-cycle distribution but harbored reduced p53 expression by 56.0% and p27 expression by 67.0%.Conclusion: 14-3-3σ may have an oncogenic function in lung adenocarcinoma but play a different role in colon cancer.