The antitumor effect of CIGB-300 peptide, a protein kinase ck2 inhibitor, in mammary cancer models

MARÍA FLORENCIA GOTTARDO; CARLA SABRINA CAPOBIANCO; JOHANNA ELENA SIDABRA; YASSER PERERA; SILVIO PEREA; DANIEL FERNANDO ALONSO; HERNAN GABRIEL FARINA

Buenos Aires

Congreso; LXII Reunión de la Sociedad Argentina de Investigación Clínica; 2017

SAIC

CK2 is a serine-threonine kinase that has been involved in growth, proliferation and cell apoptosis. CK2 has a constitutive expression and it has more than 300 substrates. In recent years, CK2 became an interesting target for anticancer therapies. Inhibition of CK2 showed antitumor activity in different types of cancer. CIGB-300 is a peptidic inhibitor of CK2, designed to bind to the phospho-acceptor domain of CK2 substrates, impairing the correct phosphorylation by the enzyme. Because breast cancer is one of the main tumor types in which CK2 is overexpressed, we focus on the effect of CK2 inhibition as a modulator of key features of breast cancer cell biology.Previously, we showed that CIGB-300 reduced the proliferation, spreading capability and ERK phosphorylation of tumor cells in a murine breast cancer model. The aim of the present study was to evaluate the role of inhibition of CK2 by CIGB-300 in murine and human mammary carcinoma cell lines. For this purpose, we evaluated the action of CIGB-300 on viability, apoptosis and clonogenic capacity using three different breast tumor cell lines, MCF7 (positive for estrogen, progesterone and HER2-neu receptors), MDA MB 231 (representative of triple negative tumors) and F3II, a murine mammary carcinoma. As compared the potential of CK2 inhibition in these models we included another chemical inhibitor of the enzyme, CX-4945. Our results showed that CIGB-300 reduced the viability of MDA MB 231 (IC50=120 μM) and MCF-7 (IC50=140 μM) (p