. ?Differential expression and localization of beta-catenin and Hsp27 after cisplatin/doxorubicin treatment in triple negative breast cancer cells?

GISELA PENNACCHIO; EVELYN CÓRDOBA; GUERRERO-GIMENEZ, MARTIN E.; MARIA M. MONTT-GUEVARA; CUELLO CARRIÓN, FERNANDO DARÍO; NADIN S; LAURA M. VARGAS-ROIG; FANELLI M

Congreso; SAN ANTONIO BREAST CANCER SYMPOSIUM; 2018

The treatment of triple-negative breast cancers (TNBC) involves the administration of theconventional chemotherapeutic drug doxorubicin, given the lack of specific targeted agents.Novel therapeutic strategies, such as cisplatin, are currently being tested for these patients.Many studies have demonstrated that aberrant Wnt/β-catenin signaling serves a role in thedevelopment of breast cancer, while others have concluded that abnormal regulation ofWnt pathway induces tumor cell chemoresistance. The small Heat shock protein 27 (Hsp27)is overexpressed in human breast cancer cells. As a result, cancer cells may suppress apoptosis and develop resistance to antineoplastic agents, such as doxorubicin. Furthermore,doxorubicin enhances cellular senescence in other tumor cell lines which is considered as atumor suppressive mechanism. Recent evidence indicates however that senescent cells secrete various growth factors and cytokines, some of which may paradoxically promote cancer progression such as TGFb, EGF, Wnt ligands, IL8, and IL6. They are known for their abilityto promote tumor progression through the inhibition of apoptosis, induction of epithelialmesenchymal transition and/or resistance to therapy. The present study sought to examinethe role of the Wnt/β-catenin and Hsp27 signaling pathway in response to cisplatin (CisPt)/doxorubicin (Doxo) treatment in human triple-negative (TN) breast cancer cell lines.