RA and ω-3 PUFA co-treatment activates autophagy in cancer cells

• DOI: 10.18632/oncotarget.22629
• Publication Date: 2017-11-23T10:46:03Z
• Authors: Shenglong Zhu; Guangxiao Lin; Ci Song; Yikuan Wu; Ninghan Feng; Wei Chen; Zhao He; Yong Q. Chen
• Keywords: 0303 health sciences; 03 medical and health sciences; Research Paper; 3. Good health

Retinoic acid (RA), is a promising therapeutic agent for the treatment of breast cancer. However, metabolic disorders and drug resistance reduce efficacy RA. In this study, we found that RA ω-3 polyunsaturated fatty acids (ω-3 PUFAs) synergistically induced cell death in vitro vivo autophagy activation. Moreover, RA-induced hypercholesterolemia was completely corrected by PUFA supplementation. addition, demonstrated effects combination on autophagic flux were independent two major canonic regulatory complexes controlling vesicle formation. The activated Gαq-p38 MAPK signaling pathways, which resulted cancer cells. Knockdown Gαq or P38 expression prevented PUFAs from inducing autophagy. Data indicated Gαq-p38activation mediated co-activation GPR40 RARα lipid rafts, rather than activation GPR120, RARβ, RARγ. results study suggest hyperlipidemic side may be ameliorated administration PUFAs. Thus, indexes corresponding drugs increased.