Effect of long-chain noncoding RNA NEAT1 on the proliferation and invasion of renal cell carcinoma

Abstract

Objective To observe the expression of long non-coding RNA (LncRNA-NEAT1) in renal cell carcinoma and cell lines, and to explore its influence on the malignant biological behavior of renal cell carcinoma and its possible molecular mechanism. Methods The expression of NEAT1 was detected by quantitative polymerase chain reaction (qPCR) in 10 cases of renal cell carcinoma and paracancerous tissues, and in 4 types of renal cell carcinoma cells and normal renal tubular epithelial cells. ACHN cells infected with negative control lentivirus (LV-NC) were used as control group, and ACHN cells infected with recombinant lentivirus carrying NEAT1 gene (LV-NEAT1) were used as experimental group. Bioinformatics predicts targeted miRNA and downstream genes of NEAT1. The effect of overexpression of NEAT1 on the mRNA expression of miR-342-3p and cell adhesion molecule 1 (CADM1) was detected by qPCR. The protein expression of CADM1 was detected by Western blot. The proliferation and invasion of ACHN cells were detected by methyl thiazolyl tetrazolium (MTT) method and Transwell invasion assay. Results The expression level of NEAT1 in renal cell carcinoma was lower than that in paracancerous tissue (P<0.01). The expression of NEAT1 in renal carcinoma cell lines was lower than that in renal tubular epithelial cells (P<0.01). After LV-NEAT1 infection, the expression of NEAT1 and CADM1 gene were significantly increased (P<0.01), while the expression of miR-342-3p decreased (P<0.01). Overexpression of NEAT1 significantly inhibited cell proliferation and invasion of ACHN cells (P<0.05). Conclusions LncRNA NEAT1 was down-regulated in renal cell carcinoma and cell lines. Overexpression of NEAT1 inhibited the proliferation and invasion of ACHN cells. The molecular mechanism may be that NEAT1 up-regulates the expression of CADM1 gene through complementary binding to miR-342-3p. Key words: RNA, long noncoding; Kidney neoplasms; Cell proliferation; Neoplasm invasiveness; In vitro