SUBCELLULAR DISTRIBUTION OF BETA-CATENIN IN CISPLATIN-TREATED TRIPLE NEGATIVE BREAST CANCER CELLS

EVELYN CÓRDOBA; GISELA PENNACCHIO; MARIANGELES AVILA MANIERO; LAURA M. VARGAS-ROIG; SILVINA NADIN; MARIEL A FANELLI

Congreso; LXII REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA (SAIC); 2017

Triple negative breast cancer subtype (TNBC) accounts for about15-20% of all invasive breast tumors. TNBC lacks expression ofestrogen receptor (ER), progesterone receptor (PR) and EpidermalGrowth Factor type 2 Receptor (HER2). To date not a singletherapy has been applied, conventional cytotoxic chemotherapy iscurrently the only treatment option for TNBC. Unfortunately, somepatients respond but others become resistant or eventually relapse.New therapeutic approaches are focused in the search of other moleculartarget and anticancer drugs not classically used for breastcancer treatment, such as platinum analogues (cisplatin). Aberrantexpression of beta-catenin has been linked to tumor progressionand has become a promising target for cancer therapy. The aim ofthis work was to study the functionality of beta-catenin exposed tocisplatin in human cell lines, MDA-MB231 (TN) and MCF10A (non- tumorigenic epithelial cell line). Cisplatin toxicity was evaluated byMTT. The localization of total and active beta-catenin was analyzedby confocal microscopy and the expression levels by WB. The IC50doses for MDA-MB231 and MCF10A were 91,48µM and 55,80µM,respectively. Cisplatin treatment induced localization of total andactive beta-catenin from the plasmatic membrane/cytoplasm to thenucleus in MDA-MB231, but no changes were observed in MCF10Acells. Expression levels of total and active beta-catenin decreasedsignificantly (p≤0,05) with cisplatin exposure in MDA-MB231 cellswhereas the levels of these proteins were not significantly modifiedin MCF10A cells. Our preliminary data show altered subcellular localizationand expression levels of beta-catenin by cisplatin in TNBCcells.