Abstract
ObjectiveLong non-coding RNAs (lncRNAs) have been identified as important players in tumorigenesis. LncRNA TMPO antisense RNA 1 (TMPO-AS1) has been shown to be involved in several tumors. However, the functional role and the underlying mechanism of TMPO-AS1 in regulating cervical cancer cell behavior remain unclear.Materials and MethodsExpression of TMPO-AS1, miR-143-3p, and ZEB1 were examined by qRT-PCR and Western blot. Cell proliferation, migration and invasion were evaluated using CCK-8 assay and Transwell migration and invasion assays, respectively. Luciferase reporter assay was performed to investigate the interaction miR-143-3p and TMPO-AS1 or ZEB1.ResultsTMPO-AS1 was highly expressed in cervical cancer cells. Furthermore, TMPO-AS1 overexpression significantly promoted C-33A cell proliferation, migration, and invasion. In contrast, TMPO-AS1 silencing inhibited SiHa cell proliferation, migration, and invasion. Mechanistically, TMPO-AS1 acted as a sponge of miR-143-3p to elevate expression of zinc finger E-box binding homeobox 1 (ZEB1), a target of miR-143-3p, and thereby promoted C-33A cell proliferation, migration, and invasion. Further assays showed that TMPO-AS1 knockdown inhibited cervical cancer cell tumorigenesis in vivo.ConclusionTMPO-AS1 promotes cervical cancer cell proliferation, migration, and invasion by regulating the miR-143-3p/ZEB1 axis.
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