POP1 promotes the progression of breast cancer through maintaining telomere integrity

Abstract

AbstractBreast cancer is one of the most common and disastrous neoplasm for women worldwide, especially triple-negative breast cancer (TNBC). Emerging evidences have demonstrated that RNase subunits are closely related to the occurrence and development of malignant tumors. However, the functions and underlying molecular mechanisms of Processing of Precursor 1 (POP1), a core component of RNase subunits, in breast cancer development have not been fully defined. Our study identified the POP1was upregulated in breast cancer cell lines and tissues and patients with higher POP1 expression were associated with poor outcomes. Overexpression of POP1 promoted cell progression in breast cancer cells, whereas silencing of POP1 induced cell cycle arrest. Moreover, Xenograft model reproduced its growth regulatory roles in breast cancer in vivo. Mechanistically, POP1 interacted and activated the telomerase complex by stabilizing the telomerase RNA component (TERC), thus protecting telomeres from shortening during division. Collectively, our findings demonstrate POP1 may as a novel prognostic marker and a therapeutic target for the management of breast cancer.