Background
Cervical cancer (CC) is one of the most common cancers in women. Long non-coding RNAs (lncRNAs) have been proposed as therapeutic targets in CC. Hence, the present study evaluated the effect of ASB16-AS1 on CC via regulating miR-1305.
Conclusions
This study reveals that ASB16-AS1 promotes cell proliferation, migration, invasion via binding miR-1305 with Wnt2, and enhancing the Wnt/β-catenin pathway. ASB16-AS1 may play a new therapeutic target for CC.
Methods
Differentially expressed lncRNAs associated with CC were screened using bioinformatics database. The expression of ASB16-AS1 and miR-1305 were measured by qRT-PCR in CC tissues and CC cells. Cell proliferation was assessed by CCK-8 and colon formation assays. Cell abilities of migration and invasion were detected by Transwell migration and invasion assays. Luciferase report assays were used to explore the correction between ASB16-AS1, miR-1305 and Wnt2 in CC. Western blot assay detect the activity of Wnt/β-catenin pathway. The xenograft tumor in nude mice was observed to evaluate tumor formation in vivo.
Results
In our study, we showed that the expression of ASB16-AS1 was increased while miR-1305 reduced was re in CC. Clinically, ASB16-AS1 and miR-1305 were correlated with poor-associated clinicopathological features of CC patients. Knockdown of ASB16-AS1 reduced CC cells proliferation, migration and invasion abilities by regulating miR-1305 in vitro and in vivo. Moreover, miR-1305 was directly bound to ASB16-AS1 and Wnt2, regulated their expression negatively. Western blot assays showed that ASB16-AS1 functioned as an oncogene by Wnt/β-catenin pathway. Conclusions: This study reveals that ASB16-AS1 promotes cell proliferation, migration, invasion via binding miR-1305 with Wnt2, and enhancing the Wnt/β-catenin pathway. ASB16-AS1 may play a new therapeutic target for CC.