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      MicroRNA‐206 has a bright application prospect in the diagnosis of cases with oral cancer


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          Previous studies have shown that microRNA‐206 ( miR‐206) exhibits anti‐tumour properties in various tumours. Nevertheless, diagnostic significance of miR‐206 in oral cancer is still poorly known. Our research was carried out to explore the performance of miR‐206 in the diagnosis of oral cancer. Quantitative real‐time polymerase chain reaction (qRT‐PCR) method was adopted to measure the level of miR‐206 in serum specimens from oral cancer cases and control individuals. Chi‐square test was performed to analyse the correlation between miR‐206 level and clinicopathological parameters of the cases. Receiver operating characteristic (ROC) curve was constituted to assess diagnostic accuracy of miR‐206 in oral cancer. Serum miR‐206 level in oral cancer patients was significantly lower than that in control individuals ( P < .001). miR‐206 expression was obviously related to T classification ( P = .033), TNM stage ( P = .008) and lymph node metastasis ( P = .028). The area under the curve (AUC) of the ROC curve was 0.846 (95% CI = 0.797‐0.896, P < .001) with a specificity of 72.7% and a sensitivity of 81.2%. It revealed that miR‐206 might be a non‐invasive indicator in differentiating oral cancer cases from control individuals. Down‐regulation of miR‐206 is related to the development of oral cancer. Serum miR‐206 might be an effective indicator for early detection of oral cancer.

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          Most cited references 28

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          Down-regulation of c-Met and Bcl2 by microRNA-206, activates apoptosis, and inhibits tumor cell proliferation, migration and colony formation

          Hsa-miRNA-206 (miR-206), highly expressed in skeletal muscle, has recently been discovered to have anticancer properties in different tissues. However, the role of miR-206 on lung cancer is still ambiguous. In this study, we investigated the role of miR-206 on the development of lung cancer. The results indicated that miR-206 expression was suppressed in lung cancer tissues and very low levels were found in non-small cell lung cancer (NSCLS) cell liness. Transient transfection of miR-206 into cultured A549 and SK-MES-1 cells led to significant decrease in cell growth, migration, invasion and colony formation, and promoted cell apoptosis. Using bioinformatics, we identified putative miR-206 binding sites within the 3′-untranslated region (3′-UTR) of the human c-Met and Bcl2 mRNA. The expression of c-Met and Bcl2 proteins were shown to be down-regulated after treated with miR-206 by subsequent Western blot and qRT-PCR analysis. Conversely, up-regulation of c-Met and Bcl2 were confirmed in tissue samples of human lung cancer, with its level inversely correlated with miR-206 expression. In addition, miR-206 also decreased the gene expression of MMP-9, CCND1 and CCND2 while increased the gene expression of p57 (Kip2) in A549 and SK-MES-1 cells. Taken together, our results demonstrated that miR-206 suppressed c-Met and Bcl2 expression in NSCLS and could function as a potent tumor suppressor in c-Met/Bcl2-over expressing tumors. Inhibition of miR-206 function could contribute to aberrant cell proliferation, migration, invasion and apoptosis, leading to NSCLS development.
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            A Serum MicroRNA Panel as Potential Biomarkers for Hepatocellular Carcinoma Related with Hepatitis B Virus

            Background The identification of new high-sensitivity and high-specificity markers for HCC are essential. We aimed to identify serum microRNAs (miRNAs) as biomarkers to be used in diagnosing hepatitis B virus (HBV) –related hepatocellular carcinoma (HCC). Methods We investigated serum miRNA expression in (261 HCC patients, 233 cirrhosis patients, and 173 healthy controls), recruited between August 2010 and June 2013. An initial screening of miRNA expression by Illumina sequencing was performed using serum samples pooled from HCC patients and controls. Quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) was used to evaluate the expression of selected miRNAs. A logistic regression model was constructed using a training cohort (n = 357) and then validated using an independent cohort (n = 241). The area under the receiver operating characteristic curve (AUC) was used to evaluate the accuracy of the use of the biomarkers for disease diagnosis. Results We identified 8 miRNAs (hsa-miR-206, hsa-miR-141-3p, hsa-miR-433-3p, hsa-miR-1228-5p, hsa-miR-199a-5p, hsa-miR-122-5p, hsa-miR-192-5p, and hsa-miR-26a-5p) and constructed an miRNA set that provided high diagnostic accuracy for HCC (AUC = 0.887 and 0.879 for training and validation sets, respectively). The miRNAs could also be used to differentiate HCC patients from healthy (AUC = 0.893) and cirrhosis (AUC = 0.892) patients. Conclusions We identified a serum of miRNA panel that has considerable clinical value in HCC diagnosis.
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              MiR-206 inhibits HGF-induced epithelial-mesenchymal transition and angiogenesis in non-small cell lung cancer via c-Met /PI3k/Akt/mTOR pathway

              MiR-206 is low expression in lung cancers and associated with cancer metastasis. However, the roles of miR-206 in epithelial-mesenchymal transition (EMT) and angiogenesis in lung cancer remain unknown. In this study, we find that hepatocyte growth factor (HGF) induces EMT, invasion and migration in A549 and 95D lung cancer cells, and these processes could be markedly inhibited by miR-206 overexpression. Moreover, we demonstrate that miR-206 directly targets c-Met and inhibits its downstream PI3k/Akt/mTOR signaling pathway. In contrast, miR-206 inhibitors promote the expression of c-Met and activate the PI3k/Akt/mTOR signaling, and this effect could be attenuated by the PI3K inhibitor. Moreover, c-Met overexpression assay further confirms the significant inhibitory effect of miR-206 on HGF-induced EMT, cell migration and invasion. Notably, we also find that miR-206 effectively inhibits HGF-induced tube formation and migration of human umbilical vein endothelial cells (HUVECs), and the mechanism is also related to inhibition of PI3k/Akt/mTOR signaling. Finally, we reveal the inhibitory effect of miR-206 on EMT and angiogenesis in xenograft tumor mice model. Taken together, miR-206 inhibits HGF-induced EMT and angiogenesis in lung cancer by suppressing c-Met/PI3k/Akt/mTOR signaling. Therefore, miR-206 might be a potential target for the therapeutic strategy against EMT and angiogenesis of lung cancer.

                Author and article information

                J Cell Mol Med
                J Cell Mol Med
                Journal of Cellular and Molecular Medicine
                John Wiley and Sons Inc. (Hoboken )
                21 August 2021
                September 2021
                : 25
                : 17 ( doiID: 10.1111/jcmm.v25.17 )
                : 8169-8173
                [ 1 ] Department of Stomatology Chinese PLA General Hospital Beijing China
                [ 2 ] Department of Prosthodontics Tianjin Stomatological Hospital Tianjin China
                [ 3 ] Department of Stomatology Beijing DCN Orthopaedic Hospital Beijing China
                [ 4 ] Otolaryngology Head and Neck Surgery Chinese PLA General Hospital Beijing China
                Author notes
                [*] [* ] Correspondence

                Lili Wang, Department of Stomatology, Chinese PLA General Hospital, Beijing, China.

                Email: tejftnd@ 123456163.com

                Shiming Yang, Otolaryngology Head and Neck Surgery, Chinese PLA General Hospital, Beijing, China.

                Email: ppuirvgjfh@ 123456163.com

                © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 2, Tables: 1, Pages: 5, Words: 3219
                Funded by: China Post‐doctoral Science Fund
                Award ID: 2018M633673
                Funded by: China Post‐doctoral Science Fund
                Award ID: 2018T111137
                Original Article
                Original Articles
                Custom metadata
                September 2021
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.7 mode:remove_FC converted:05.09.2021

                Molecular medicine

                diagnosis, mir‐206, oral cancer


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