유방암 세포에서 CAGE에 의한 Autophagy 조절과 항암제 내성의 증진

We established anti-cancer drug-resistant breast cancer cells (MCF7R)by exposing MCF7 cells to increasing concentrations of celastrol .MCF7R cells showed higher expression of CAGE, a cancer/testis antigen, and autophagic fluxes, such as pBeclin1Ser15 and LC3 than MCF7 cells. CAGE showed an interaction with Beclin1 in MCF7R cells. MCF7R cells showed higher LC3 puncta expression than MCF7 cells. The down-regulation of CAGE enhanced sensitivity to various anti-cancer drugs in MCF7R cells while overexpression of CAGE conferred resistance to anti-cancer drugs in MCF7 cells. We found that Dead –bo x domain of CAGE was necessary for regulating the expression of autophagic fluxes in breast cancer cells. Overexpression of CAGE increased LC3 puncta expression in MCF7 cells. MCF7R cells showed higher invasion, migration potential and growth rate than MCF7 cells. We present evidence that anti-cancer drug-resistance is accompanied by promotion of autophagy and CAGE is necessary for anti-cancer drug-resistance and autophagy in breast cancer cells