Knockdown of LINC01123 inhibits cell viability, migration and invasion via miR-361-3p/TSPAN1 targeting in cervical cancer.

Abstract

Cervical cancer (CC) is a type of gynecological malignancy that poses a significant threat to females. The aim of the present study was to examine the role of long intergenic non-protein coding RNA 1123 (LINC01123) and its underlying molecular mechanism in the development of CC. mRNA expression levels of LINC01123 and microRNA (miR)-361-3p in CC tissue samples and cell lines were evaluated using reverse transcription-quantitative PCR. Cell viability, migration and invasion were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing and Transwell assays. Moreover, a xenograft tumor model was established for elucidating the influence of LINC01123 knockdown on tumor growth in vivo. A dual-luciferase reporter assay was used to confirm the association between LINC01123 and miR-361-3p, and miR-361-3p and tetraspanin 1 (TSPAN1). Western blot analysis was used to determine TSPAN1 protein expression. LINC01123 expression was upregulated and miR-361-3p expression was reduced in CC tissue samples and cell lines. Knockdown of LINC01123 inhibited cell viability, migration and invasion in vitro, and suppressed tumor growth in vivo. Furthermore, LINC01123 targeted miR-361-3p and negatively regulated miR-361-3p expression. Overexpression of miR-361-3p inhibited cell viability, migration and invasion in HeLa and CaSki cells. Additionally, miR-361-3p targeted TSPAN1 and negatively regulated TSPAN1 expression. Inhibition of miR-361-3p and overexpression of TSPAN1 reversed the effect of LINC01123 knockdown on cell proliferation, migration and invasion in HeLa cells. Knockdown of LINC01123 inhibited cell proliferation, migration and invasion via miR-361-3p/TSPAN1 regulation in CC, which may present an effective target for treatment of CC.