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

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 . 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 , and suppressed tumor growth . 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.