Long non-coding RNAs (lncRNAs) may serve as miRNA sponges to modulate the expressions of miRNA target genes. LncRNA X-inactive specific transcript (XIST) has been demonstrated to be upregulated and act as an oncogene in non-small cell lung cancer (NSCLC). However, the sponge role of XIST in NSCLC progression remains largely unknown. In this study, we demonstrated that XIST was substantially upregulated and miR-137 was aberrantly downregulated in NSCLC tissues and cells. XIST was identified to function as a competitive endogenous RNA (ceRNA) for miR-137 to promote NSCLC cell viability and invasion. Additionally, our results suggested that miR-137 targeted the 3'UTR of paxillin (PXN) to suppress NSCLC cell viability and invasion. Meanwhile, miR-137 was negatively correlated with PXN expression while XIST was positively correlated with PXN expression. More importantly, XIST positively regulated PXN levels by sponging miR-137 in vitro and in vivo. Collectively, our study provided the evidence for the cross-talk between XIST, miR-137, and PXN, shedding light on the therapy for NSCLC.
Keywords: Invasion; NSCLC; Paxillin; Viability; XIST; lncRNA; miR-137.
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