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Background Radiation resistance is a major obstacle to the prognosis of cervical cancer (CC) patients. Many studies have confirmed that long non-coding RNAs (lncRNAs) are involved in the regulation of radiosensitivity of cancers. However, whether small nucleolar RNA host gene 12 (SNHG12) regulates the radiosensitivity of CC remains unknown. Methods Quantitative real-time polymerase chain reaction was used to measure the expression levels of SNHG12 and microRNA-148a (miR-148a). The radiosensitivity of cells was evaluated by clonogenic assay. Flow cytometry and caspase-3 activity assay were performed to assess the apoptosis ability and cell cycle distribution of cells. Besides, dual-luciferase reporter and RNA immunoprecipitation assay were used to verify the interaction between miR-148a and SNHG12 or cyclin-dependent kinase 1 (CDK1). Also, the protein levels of CDK1, CCND1 and γ-H2AX were detected by western blot analysis. Furthermore, in vivo experiments were conducted to verify the effect of SNHG12 on CC tumor growth. Ki-67 and TUNEL staining were employed to evaluate the proliferation and apoptosis rates in vivo. The hematoxylin and eosin (HE) staining were employed to evaluate the tumor cell morphology. Results SNHG12 was upregulated in CC tissues and cells, and its knockdown improved the radiosensitivity by promoting the radiation-induced apoptosis and cell cycle arrest of CC cells. Also, miR-148a could be sponged by SNHG12 and could target CDK1. MiR-148a inhibitor or CDK1 overexpression could invert the promotion effect of silenced-SNHG12 on CC radiosensitivity. Meanwhile, SNHG12 interference reduced the tumor growth of CC, increased miR-148a expression, and inhibited CDK1 level in vivo. Conclusion LncRNA SNHG12 promoted CDK1 expression to regulate the sensitivity of CC cells to radiation through sponging miR-148a, indicating that SNHG12 could be used as a potential biomarker to treat the radiotherapy resistance of CC patients.

Increasing evidence revealed that circular RNAs (circRNAs) play important roles in tumor progression. In the present study, we explored the roles and underlying mechanisms of hsa_circ_0075341 in cervical cancer development. Our data showed that the expression of hsa_circ_0075341 was significantly upregulated and associated with larger tumor size, advanced FIGO stage, and lymph-node metastasis in cervical cancer patients. Hsa_circ_0075341 inhibition reduced cervical cancer cell proliferation and invasion in vitro. In mechanism, hsa_circ_0075341 negatively regulated miR-149-5p in cervical cancer progression. In addition, AURKA was confirmed as a direct target of miR-149-5p in cervical cancer and positively regulated by hsa_circ_0075341. Collectively, our data suggested that hsa_circ_0075341 promoted cervical cancer cell proliferation and invasion through regulating the miR-149-5p/AURKA axis, which provided a novel therapeutic target for cervical cancer treatment.

Introduction Long non-coding RNAs (lncRNAs) have been shown to have great importance in cancer development and progression. However, the mechanism of lncRNAs in epithelial ovarian cancer remains unclear. In the present study, we aimed to explore the role of the lncRNA myocardial infarction-associated transcript (MIAT) in epithelial ovarian cancer tumorigenesis. Material and methods Quantitative real-time PCR (qRT-PCR) was used to determine MIAT expression in human epithelial ovarian cancer tissues and cell lines, and the effects of MIAT on cell proliferation and cell apoptosis were determined by CCK-8 assay or flow cytometry analysis. Dual-Luciferase Reporter assay and Western blot assay were used to explore the molecular mechanisms of MIAT in epithelial ovarian cancer cells progression. Results Our data showed that the expression of lncRNA MIAT was remarkably increased in human epithelial ovarian cancer tissues and cell lines (p < 0.05). High MIAT expression was associated with poor overall survival of epithelial ovarian cancer patients (p < 0.05). Function assays showed that knockdown of MIAT expression significantly inhibited epithelial ovarian cancer cell proliferation and promoted cell apoptosis in vitro (p < 0.05). Moreover, we revealed that MIAT might function as an endogenous miR-330-5p sponge to regulate the target gene of miR-330-5p in epithelial ovarian cancer progression. Conclusions LncRNA MIAT was found to be a tumor oncogenic lncRNA in epithelial ovarian cancer tumorigenesis. LncRNA MIAT promoted cell proliferation and inhibited cell apoptosis by negative regulation of miR-330-5p in epithelial ovarian cancer cells. Our findings suggested that MIAT might act as a candidate prognostic biomarker and new therapeutic target for treating epithelial ovarian cancer patients.

Long non-coding RNAs (lncRNAs) play important roles in tumor initiation and progression, including cervical cancer (CC). However, the effects and underlying mechanisms of STXBP5-AS1 in CC are still unknown. The expression of STXBP5-AS1, miR-96-5p, and PTEN in CC was explored by qRT-PCR. CCK-8 and transwell assays were used to determine the roles of STXBP5-AS1 on CC progression. Luciferase report assay and RIP assay were used to explore the correction between STXBP5-AS1, miR-96-5p and PTEN in CC. In our study, we showed that the expression of STXBP5-AS1 and PTEN was reduced while miR-96-5p expression was upregulated in CC. STXBP5-AS1 overexpression significantly reduced CC cells proliferation and invasion ability by suppressing miR-96-5p expression. MiR-96-5p promoted CC cells progression via regulating PTEN expression. Furthermore, STXBP5-AS1 was identified as a ceRNA to upregulate PTEN via sponging miR-96-5p in CC. Taken together, our findings revealed that STXBP5-AS1 might function as a ceRNA to drive CC cells proliferation and invasion via regulating miR-96-5p/PTEN axis.