Carvacrol Induces Doxorubicin-Resistant Breast Cancer Cell Apoptosis via Inhibition of the PI3K/Akt Pathway
Carvacrol Induces Doxorubicin-Resistant Breast Cancer Cell Apoptosis via Inhibition of the PI3K/Akt Pathway
Hu-Hu Chen1,2*, Jiao-han Zhou3 and Siat Yee Fong2,4
ABSTRACT
Doxorubicin (Dox), a widely used chemotherapeutic agent for breast cancer, is often ineffective due to the development of Dox resistance, posing a significant challenge in cancer treatment. Carvacrol is a monoterpene phenol with diverse biological activities, has emerged as a potential anticancer agent. However, its antitumor effects and underlying mechanism against Dox-resistant breast cancer remain largely unexplored. This study investigated the effect of carvacrol on cell viability, cell cycle progression, and apoptosis in Dox-resistant triple negative breast cancer (TNBC) MDA-MB-231/Dox cells. Western blotting analyses were performed to access protein levels associated with apoptosis and the PI3K/Akt pathway. The results revealed that carvacrol significantly inhibited MDA-MB-231/Dox cell proliferation in a concentration-dependent manner compared to the control (p <0.05). Furthermore, carvacrol treatment increased the distribution of MDA-MB-231/Dox cells in the G0/G1 phase while decreasing the distribution in the S and G2/M phases (p <0.05). Moreover, carvacrol treatment enhanced the apoptosis rate and Bax protein expression, while decreasing Bcl-2, PI3K and P-Akt protein levels, indicating that carvacrol treatment induced cell apoptosis by deactivating the PI3K/Akt signaling pathway. These findings suggest that carvacrol holds promise as a therapeutic strategy for Dox-resistant breast cancer, providing novel insights into the development of effective therapies that address drug resistance and improve patient outcomes.
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