Long noncoding RNA LINP1 acts as an oncogene and promotes chemoresistance in breast cancer.

Recent studies have shown that long non-coding RNAs (lncRNAs) are involved in a number of biological processes; however, further study is still warranted to comprehensively reveal their functions. In this study, we showed that the lncRNA in non-homologous end joining (NHEJ) pathway 1 (LINP1) was related to breast cancer cell proliferation, metastasis and chemoresistance. Loss- and gain-of function studies were used to assess the role of LINP1 in promoting breast cancer progression. LINP1 knockdown mitigated breast cancer cell growth by inducing G1-phase cell cycle arrest and apoptosis. LINP1 also promoted breast cancer cell metastasis and influenced the expression of epithelial-mesenchymal transition-related markers. We identified p53 as a regulator of LINP1, and LINP1 overexpression could restore the metastatic effects of p53. Furthermore, LINP1 was upregulated in doxorubicin- and 5-fluorouracil-resistant cells and induced chemoresistance. We also observed that LINP1 enrichment played a critical functional role in chemoresistance by inhibiting chemotherapeutics-induced apoptosis. Moreover, LINP1 in tumors was associated with lower overall survival and disease-free survival. In conclusion, LINP1 may serve as a potential oncogene and chemoresistance-related regulator of breast cancer cells, suggesting that LINP1 might be a potent therapeutic target and might reduce chemoresistance in breast cancer.