Abstract
Long noncoding RNA (lnc RNA) is aberrant expressed in many kinds of tumors and may be concerned with the occurrence and progression of tumors. Lnc RNA MST1P2 is increased in cervical cancer (CC), but its mechanism in CC has not been clarified. In this study, RT-qPCR was employed to analyze Lnc MST1P2 and miR-133b expression. CCK8 and cell apoptosis assay detect the proliferation optical density (OD) value and apoptosis rate. Cell metastasis was evaluated by Wound-healing assay and Transwell assay. Dual-Luciferase assay analyzed the relationship between Lnc MST1P2 and miR-133b. In vivo experiment was performed by establishing xenograft animal model. We found that Lnc MST1P2 is obviously overexpression in CC tissues and cells. Si-Lnc MST1P2 obviously repressed cell growth, cell migration, and cell invasion in Hela and SIHA cells. Moreover, Si-Lnc MST1P2 suppressed CC tumorigenesis in vivo. Dual-Luciferase assay and RT-qPCR assay further proved that Lnc MST1P2 has a negative regulation to miR-133b. miR-133b up-regulation inhibited cell viability and metastasis of Hela and SIHA cells. miR-133b inhibition notably decreased the anti-cancer effect of si-Lnc MST1P2. LncRNA MST1P2 serves as a Cervical Cancer oncogene by sponging with miR-133b.