There is a growing body of evidence indicating that long non-coding RNAs (lncRNAs) are associated with a variety of cancers. LncRNA LINP1 has been shown to be a key factor in tumor malignancy. However, the role of LINP1 in cervical cancer (CC) it is unclear. In our research, we found that the levels of LINP1 were significantly elevated in CC tissues by comparison with adjacent normal tissue. Further, the expression level of LINP1 was upregulated in CC cells compared with healthy human cervical epithelial cell lines (HUCEC). Surprisingly, we found that downregulation of LINP1 significantly reduced the proliferation of CC cells and promoted apoptosis. Additionally, downregulation of LINP1 significantly decreased CC tumor growth in vivo. Further, we observed that LINP1 recruits EZH2, LSD1, and DNMT1, thereby reducing the expression of KLF2 and PRSS8. The results from our qRT-PCR analyses showed that silencing LINP1 uprgulated the expression of KLF2 and PRSS8 in CC cells. The results from our loss-of-function assays showed that upregulation of KLF2 and PRSS8 inhibits cell proliferation and boosts cell apoptosis in CC. We also found that inhibition of KLF2 and PRSS8 reversed the inhibitory effect on cell proliferation associated with silencing LINP1. In short, LINP1 facilitates the progression of CC by suppressing KLF2 and PRSS8, and thus could provide a promising target for CC therapy.
Keywords: KLF2; LINP1; PRSS8; cancer du col utérin; cervical cancer.