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Correlation between microRNA (miRNA)-206 and miRNA-145 expression and prognosis in breast cancer was investigated. Breast cancer specimens and paracancerous tissues of 372 breast cancer patients who underwent surgical resection in the First Affiliated Hospital of Shantou University Medical College from September 2010 to September 2014 were included. qRT-PCR was used to detect the expression of miR-206 and miR-145 in breast cancer and paracancerous tissues, and patients were divided into high and low expression groups according to the median expression level to plot survival curve. Expression levels of miR-145 and miR-206 in breast cancer tissues were 2.24±1.23 and 0.76±0.24, respectively. Expression level of miR-145 was significantly lower, while expression level of miR-206 was significantly higher in tumor tissues than in paracancerous tissues (p<0.05). The 3-year survival rates of miR-145 low expression group and miR-206 high expression group were also lower than that of miR-145 high expression group and miR-206 low expression group, respectively (p<0.05). Expression of miR-206 is upregulated and expression of miR-145 is downregulated in breast cancer, which may have an impact on the prognosis of patients. miR-206 and miR-145 may serve as important indicators to predict prognosis of patients with breast cancer in the future. [ABSTRACT FROM AUTHOR]

Cervical cancer (CC) is one of the most frequent gynecological malignancies in females worldwide. Aberrant expression of microRNA (miR)-206 was reported to play an important role in tumor progression. The aim of the present study was to evaluate the potential role of miR-206 and verify its influence on the function of glucose-6-phosphate dehydrogenase (G6PD) in CC. Western blot analysis and RT-PCR were employed to measure miR-206 and G6PD expression. Luciferase assays were performed to validate G6PD as miR-206 targets. CCK-8 assay was performed to examine the regulation of miR-206 and G6PD on CC proliferation. The result showed that miR-206 was downregulated, while G6PD was upregulated in high risk human papillomavirus (HR-HPV)(+) CC. miR-206 directly targeted the 3′-UTR of G6PD. miR-206 overexpressed or G6PD low-expressed suppressed cell proliferation. miR-206 low expressed or G6PD overexpressed predicted poor prognosis. In conclusion, miR-206 reduced cancer growth and suppresses the G6PD expression in CC. This newly identified miR-206 may provide further insight into tumor progression and offers a promising target for the CC therapy. [ABSTRACT FROM AUTHOR]

Legg-Calvé-Perthes disease (LCPD) commonly onsets in adolescents, and threatens their health. However, the potential mechanism underlying LCPD remains unclear. MicroRNA (miR)-206 and SRY-box 9 (SOX9) serve an important role in chondrocytes; however, their role in LCPD remains ambiguous. In the present study, whether miR-206 and SOX9 mediated cell apoptosis in dexamethasone (DEX)-induced LCPD was investigated. The chondrocytes of the LCPD and normal control group were isolated from clinical tissues. Reverse transcription-quantitative polymerase chain reaction was used to evaluate the expression of miR-206 and SOX9 mRNA. Western blotting was used to measure the protein level of SOX9. A combination of Annexin V-fluorescein isothiocyanate flow cytometry was used to assess cell apoptosis. The association between miR-206 and SOX9 was detected using a luciferase reporter assay. miR-206 was overexpressed while SOX9 was downregulated in chondrocytes treated with DEX obtained from patients with LCPD. miR-206 targeted SOX9 to regulate its expression. Overexpression of miR-206 promoted cell apoptosis in TC28, while it was reversed by SOX9 overexpression. TC28 cells pretreated with DEX significantly promoted cell apoptosis, while cells transfected with miR-206 inhibitor significantly reversed the effect; however, downregulated SOX9 abolished the effects of miR-206 inhibitor. SOX9 mediated by miR-206 possibly contributed to the pathogenesis of LCPD. The results of the present study suggest that miR-206 and SOX9 function as important therapeutic targets for the future of clinical therapy. [ABSTRACT FROM AUTHOR]

MicroRNA (miRNA)-based targeting in cancer has emerged as a potential therapeutic strategy. miR-206 has recently been implicated in cancer. However, the role and molecular mechanism of miR-206 in lung adenocarcinoma are still unclear. The present study revealed that miR-206 was downregulated in human lung adenocarcinoma tissues. Overexpression of miR-206 in human lung adenocarcinoma-derived cells significantly inhibited cell viability and migration. Further experiments indicated that the overexpression of miR-206 decreased the expression of MET at the messenger RNA and protein levels via direct targeting of MET in a 3'-untranslated region-dependent manner. The knockdown of MET by small interfering RNA partly led to a phenocopy effect of miR-206. In conclusion, the present study identified miR-206 as a potential tumor suppressor of lung adenocarcinoma that exerts its functions, in part, by negative regulation of MET. [ABSTRACT FROM AUTHOR]

MicroRNA (miRNA)-based targeting in cancer has emerged as a potential therapeutic strategy. miR-206 has recently been implicated in cancer. However, the role and molecular mechanism of miR-206 in lung adenocarcinoma are still unclear. The present study revealed that miR-206 was downregulated in human lung adenocarcinoma tissues. Overexpression of miR-206 in human lung adenocarcinoma-derived cells significantly inhibited cell viability and migration. Further experiments indicated that the overexpression of miR-206 decreased the expression of MET at the messenger RNA and protein levels via direct targeting of MET in a 3'-untranslated region-dependent manner. The knockdown of MET by small interfering RNA partly led to a phenocopy effect of miR-206. In conclusion, the present study identified miR-206 as a potential tumor suppressor of lung adenocarcinoma that exerts its functions, in part, by negative regulation of MET.