DEPDC1, negatively regulated by miR-26b, facilitates cell proliferation via the up-regulation of FOXM1 expression in TNBC.

Abstract

Triple negative breast cancer (TNBC), characterized by lack of estrogen receptors, progesterone hormone receptors, and HER2 overexpression, is a more aggressive high grade tumor and not sensitive to current targeted drugs. The clinical prognosis of TNBC is poorer than other types of breast cancer, and there is no effective therapy strategy until now. Thus, it is necessary to determine important factors involved in regulating the progression of TNBC. In this study, we found DEPDC1 was up-regulated in the tissues of TNBC compared with their paired peritumoral tissues. DEPDC1 over-expression facilitated cell proliferation and tumor growth through increasing the expression of FOXM1 in TNBC cells. Conversely, knockdown of DEPDC1 had the opposite effects. Moreover, miR-26b, acting as a tumor suppressor in TNBC, directly repressed the expression of DEPDC1 and mitigated its promotive effects on cell growth and colony formation. These results indicate that DEPDC1, negatively regulated by miR-26b, promotes cell proliferation and tumor growth via up-regulating FOXM1 expression, implying an important underlying mechanism of regulating the progression of TNBC.