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Abstract
BackgroundLong noncoding RNAs (lncRNAs) play key roles in cancer development. The lncRNA miR-497 host gene (MIR497HG) has been identified to slow tumor progression in several cancers. This study aims to identify the effect of MIR497HG on cervical cancer (CC) progression and explore the underlying mechanism. MethodsThe effect of MIR497HG on CC cell growth, apoptosis, migration, and invasion were examined by CCK-8, colony formation, flow cytometry, wound healing, and transwell assays. Western blotting, RT-qPCR, and luciferase reporter assays as well as bioinformatics prediction websites were used to explore the molecular mechanism how MIR497HG modulates B cell CLL/lymphoma 6 member B (BCL6B) expression to regulate PI3K/AKT pathway. The clinical specimens of CC were collected to test the gene expression and prognostic values of MIR497HG, BCL6B, and miR-7-5p. The xenograft CC model was established by subcutaneous transplantation of human CC cell lines. Xenograft tumors were used to detect the expression of BCL6B and PI3K/AKT signaling by immunohistochemistry. ResultsMIR497HG expression was downregulated in CC tissues and cells. MIR497HG overexpression inhibited cell proliferation, migration, and invasion, and facilitated apoptosis. MIR497HG blocked PI3K/AKT signaling pathway by upregulating BCL6B expression in CC cells. MIR497HG upregulated BCL6B expression by sponging miR-7-5p. BCL6B knockdown, or miR-7-5p overexpression reversed the antitumor effect of MIR497HG on CC. Additionally, abnormal expressions of MIR497HG, BCL6B, and miR-7-5p were all associated with the survival outcomes of CC patients. The results in in vivo xenograft tumor models showed that MIR497HG overexpression inhibited CC growth via the miR-7-5p/BCL6B/PI3K/AKT axis. ConclusionOverall, MIR497HG inhibits CC development and progression by upregulating BCL6B to block PI3K/AKT pathway, implicating that MIR497HG might be an effective therapeutic target for CC.
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