Metabolic reprogramming is thought to be one of the initiators in
cancer drug resistance. It has been shown that
CTAB is capable of interfering the efficiency of
cancer therapy by regulation of cell metabolic reprogramming. In this study, we hypothesized that AMPK as a key metabolic regulator plays a crucial role in regulation of
breast cancer drug resistance, which could be alleviated by treatment of
CTAB. We observed that
CTAB can improve the DOX sensitivity of the
breast cancer cells by inhibition of the
ATP-dependent
drug-efflux pump P-gp complex through activation of the AMPK-HIF-1α-P-gp cascades. The
CTAB effect was also confirmed in vivo showing low systemic toxicity. Taken together, our results showed that
CTAB sensitized drug resistance of
breast cancer to DOX
chemotherapy by activating AMPK signaling cascades both in vitro and in vivo, suggested that
CTAB may be developed as a promising and novel chemosensitizer and chemotherapeutic candidate for
breast cancer treatment.