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MicroRNAs (miRNAs/miRs) are short non-coding RNAs (between 20 and 22 nucleotides) that regulate gene expression by binding to the 3'-untranslated region of target mRNA, and preventing protein translation or inducing mRNA destabilization. miRNAs are predicted to target ~60% of all mRNAs, therefore providing a marked degree of regulation of a number of cellular processes. In the present study, the expression of miR-548c-3p was determined by reverse transcription-quantitative polymerase chain reaction analysis and demonstrated to be markedly downregulated in clinical malignant glioma tissues and the glioma T98G cell line compared with normal human brain tissue. Transfection of miR-548c-3p inhibited cell proliferation by inducing G1 cell cycle arrest and also inhibited the migration of the T98G cells in vitro. Furthermore, a bioinformatic algorithm and a luciferase reporter assay identified proto-oncogene c-Myb (c-Myb) as a potential direct target of miR-548c-3p. Further experiments demonstrated that the inhibition of c-Myb by miR-548c-3p partially mediated the antitumor effect of miR-548c-3p. The results of the present study provide the novel insight that miR-548c-3p inhibits glioma tumorigenesis by targeting c-Myb. Therefore, miR-548c-3p may contribute to the development of improved glioma treatment. [ABSTRACT FROM AUTHOR]

Cervical cancer is the second most common malignancy in women worldwide and always has recurrence owing to radioresistance. MicroRNA (miRNA or miR) has been identified to relate to the sensitivity of cancer radiotherapy. Here, we investigated the potential of miRNA-320 as a biomarker for radiosensitivity by targeting β-catenin in cervical cancer. A radioresistant cervical cancer cell line, C33AR, was established, and the radioresistance of C33AR cells was confirmed by a colony-formation assay. The expression of miRNA-320 was detected by reverse transcription-quantitative polymerase chain reaction, and compared between C33A and C33AR. β-catenin, the target of miRNA-320, was determined at the protein level by western blotting after transfecting the inhibitor of miRNA-320. The expression of miRNA-320 was markedly decreased in C33AR cells, which appeared to be more radioresistant, compared with its parental cell line C33A. Target prediction suggested that miRNA-320 negatively regulated the expression of β-catenin. Knockdown of β-catenin increased C33AR radiosensitivity, which revealed that the inhibition of β-catenin could rescue the miRNA-320-mediated cell radioresistance. On the other hand, overexpressing miRNA-320 increased C33AR radiosensitivity. In conclusion, miRNA-320 regulated the radiosensitivity of C33AR cells by targeting β-catenin. This finding provides evidence that miRNA-320 may be a potential biomarker of radiosensitivity in cervical cancer. [ABSTRACT FROM AUTHOR]

Ovarian cancer is one of the most common types of gynecological malignancy worldwide, and is the fourth leading cause of cancer-associated mortality among women. Despite improvements in therapeutic treatments, the prognosis for epithelial ovarian cancer (EOC) remains poor, mainly due to the rapid growth and metastasis of ovarian cancer tumors. An increasing number of studies have indicated that microRNAs (miRNAs) are involved in the carcinogenesis and progression of human cancer, suggesting that miRNAs may be used in clinical prognosis and as a therapeutic target in EOC. The aim of the present study was to investigate the expression levels of miRNA-494 in EOC tissues and cell lines. The clinical significance of miRNA-494 in patients with EOC was also evaluated. The results demonstrated that miRNA-494 was significantly downregulated in EOC tissues and cell lines. Low expression levels of miRNA-494 were associated with poor prognostic features, including International Federation of Gynecology and Obstetrics stage, tumor size and lymph node metastasis. In vitro functional studies demonstrated that overexpression of miRNA-494 inhibited proliferation, migration and invasion in EOC cells. By contrast, knockdown of miRNA-494 enhanced cell growth, migration and invasion in EOC cells. Notably, sirtuin 1 (SIRT1) was identified as a direct target of miRNA-494 in EOC. Furthermore, MTT, cell migration and invasion assays verified that EOC cell proliferation, migration and invasion were completely restored with forced miRNA-494 expression and SIRT1 restoration. Together, these findings suggest that miRNA-494 is a potential prognostic marker, and may provide novel therapeutic regimens of targeted therapy for EOC. [ABSTRACT FROM AUTHOR]

Our previous study revealed that miR-148a, a cyclic adenosine monophosphate-response element binding protein-modulated microRNA that promotes adipocyte differentiation by inhibiting Wnt1, is a biomarker of obesity in human subjects and a mouse model. The present study investigated the expression of miR-148a in human adipose tissue-derived mesenchymal stem cells (hMSCs-Ad) in response to inflammatory cytokines and adipokines to clarify its underlying mechanism. miR-148a expression was detected using reverse transcription-quantitative polymerase chain reaction analysis and its promoter activity was detected with a luciferase assay. miR-148a expression levels decreased when differentiated hMSCs-Ad were exposed to inflammatory cytokines or adipokines, which suggested that miR-148a may be important in adipocyte metabolism and inflammation. Furthermore, the promoter activity of miR-148a decreased following treatment of cells with inflammatory cytokines or adipokines. The results of the present study indicated a novel role of miR-148a in adipocyte inflammation; therefore, miR-148a may be involved in obesity complications via its own underlying transcriptional mechanism. [ABSTRACT FROM AUTHOR]

The function of microRNAs (miRNAs) in tumorigenesis has been extensively investigated. In the present study, the aim was to investigate the expression and role of miR-204 in B-cell lymphoma. The present study demonstrated that miR-204 is downregulated in B-cell lymphoma. Using in vitro studies, overexpression of miR-204 was shown to inhibit growth in Daudi and Raji B-cell lymphoma cell lines. Furthermore, miR-204 could bind the 3'-untranslated region of signal transducer activator of transcription 5 (STAT5), a transcription factor that promotes B-cell lymphoma oncogenesis. Re-introduction of STAT5 reversed the antiproliferative roles of miR-204, confirming the specific importance of STAT5 for miR-204 action in cell proliferation. The present study suggests a novel mechanism for dysregulated miRNAs in the progression of B-cell lymphoma. [ABSTRACT FROM AUTHOR]