Efp promotes growth of triple-negative breast cancer cells

Abstract

Triple-negative breast cancer (TNBC) is characterized by its high ability of invasiveness and metastasis, namely lacking expression of estrogen receptor (ER), progesterone receptor, and HER2. We previously demonstrated that estrogen responsive finger protein (Efp) plays a tumor-promotive role in ER-positive breast cancer, yet it remains to be addressed whether Efp contributes to TNBC pathophysiology. We here found that Efp mRNA and protein were abundantly expressed in TNBC patient-derived cells and MDA-MB-231 cells. Efp silencing significantly decreased the growth and migration of both TNBC cell models. Cell-cycle profiling showed a decrease in the S phase population upon Efp silencing. Moreover, exogenous Efp expression increased the growth, migration, and the percentages of S phase population of TNBC cells. Transcriptomic analysis in the Efp-silenced TNBC cells identified several candidate Efp targets including cell cycle-related genes CDCA7 and HELLS, whose contribution to cell growth were validated by siRNA-mediated gene silencing. These results suggest that Efp plays a tumor-promotive role in TNBC and can be a potential therapeutic target for the aggressive disease.