Downregulation of GATS gene inhibits proliferation, clonogenicity and migration in triple negative breast cancer cells MDA-MB-231 by cell autophagy.

Abstract

The triple negative breast cancer (TNBC) accounts for 15% to 20% of the total number of breast cancer diagnosed. A number of clinical studies have shown that TNBC has a high risk of early recurrence and distant metastasis, and a low rate of disease free survival and total survival. The premise of TNBC deterioration was abnormal proliferation and migration of tumor cells, and this study firstly showed that GATS gene could promote proliferation of MDA-MB-231 breast cancer cells. Through lentiviral expression system, the GATS gene was konckdown by shGATS lentivirus infection in the MDA-MB-231 cells, and the result indicated it could remarkably decrease the ability of cell proliferation and migration. Real-time PCR, western blot and immunofluorescence experiments showed the expressions of protein LC3, and p-Akt in shGATS cell group were lower than the shCtrl group. Therefore, we suggest the GATS could promote the MDA-MB-231 cell proliferation, migration and clonogenicity through cell autophagy by the PI3K/Akt pathway, which paved the way for further study the function of GATS in TNBC, and GATS may potentially be a target for gene therapy against triple negative breast cancer.