Abstract
ObjectiveLong non-coding RNAs (lncRNAs) have been identified as important players in tumorigenesis. LncRNA highly upregulated in liver cancer (HULC) has been identified as a key regulator in the progression of various cancers. However, the functional role and the mechanisms of HULC in regulating cervical cancer cell behavior remain unclear.MethodsHULC expression, miR-218 expression and TPD52 mRNA level in cervical cancer cells were examined by qRT-PCR. Cell proliferation was evaluated by MTT assay. Cell migration and invasion were examined by Transwell assay. TPD52 protein level was measured by Western blot. Dual-luciferase reporter assay was measured to verify the combination of HULC and miR-218 as well as miR-218 and TPD52.ResultsHULC expression was upregulated in cervical cancer cell lines, and HULC promoted cervical cancer cell proliferation, migration and invasion. Mechanistically, HULC acted as a sponge of miR-218 to elevate expression of TPD52, a target of miR-218, and thereby promoted cervical cancer cell proliferation, migration, and invasion.ConclusionHULC promotes cervical cancer cell proliferation, migration and invasion via miR-218/TPD52 axis.
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