A novel long non-coding RNA-PRLB acts as a tumor promoter through regulating miR-4766-5p/SIRT1 axis in breast cancer

作者：Liang, Yiran; Song, Xiaojin; Li, Yaming; Sang, Yuting; Zhang, Ning; Zhang, Hanwen; Liu, Ying; Duan, Yi; Chen, Bing; Guo, Renbo; Zhao, Wenjing; Wang, Lijuan; Yang, Qifeng^*

来源：Cell Death & Disease, 2018, 9(5): 563.

DOI：10.1038/s41419-018-0582-1

• COMPETING ENDOGENOUS RNA
• WNT/BETA-CATENIN
• CELL APOPTOSIS
• METASTASIS
• PROGRESSION
• RESISTANCE
• SIRT1
• CHEMORESISTANCE
• PROLIFERATION
• ANGIOGENESIS

Accumulating evidence indicates that long non-coding RNAs (IncRNAs) play a critical role in cancerous processes as either oncogenes or tumor suppressor genes. Here, we demonstrated that IncRNA-PRLB (progression-associated IncRNA in breast cancer) was upregulated in human breast cancer tissues and breast cancer cell lines. Further evaluation verified that IncRNA-PRLB was positively correlated with the extent of metastasis, and its expression was correlated with shorter survival time of breast cancer patients. We identified microRNA miR-4766-5p as an inhibitory target of IncRNA-PRLB. Both IncRNA-PRLB overexpression and miR-4766-5p knockdown could remarkably enhance cell growth, metastasis, and chemoresistance. We also determined that sirtuin 1 (SIRT1) was an inhibitory target of miR-4766-5p, and that SIRT1 was inhibited by both IncRNA-PRLB knockdown and miR-4766-5p overexpression. Significantly, we found that the promotion of cell proliferation and metastasis, the acquisition of chemoresistance, and the increased expression of SIRT1 induced by IncRNA-PRLB overexpression could be partly abrogated by ectopic expression of miR-4766-5p. Taken together, our findings indicated that IncRNA could regulate the progression and chemoresistance of breast cancer via modulating the expression levels of miR-4766-5p and SIRT1, which may have a pivotal role in breast cancer treatment and prognosis prediction.

• 出版日期2018-5-11
• 单位山东大学