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      miR-206 Inhibits Laryngeal Carcinoma Cell Multiplication, Migration, and Invasion

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          Abstract

          Laryngeal carcinoma (LC) is one of the common human cancer types. MicroRNAs (miRNAs) were reported to be the essential regulators in cancer diagnosis, treatment, and prognosis. It was reported that miR-206 expression was reduced in various neoplastic diseases. However, the role and functional mechanism of miR-206 in LC progression remain unclear. In this research, miR-206 was found to be associated with tumor-node-metastasis (TNM) staging. In addition, the area under the curve (AUC) of miR-206 was 0.902 for diagnosis of LC and 0.854 for differential diagnosis of stage I-II and stage III-IV patients. Low expression of miR-206 was associated with poor prognosis of LC patients. miR-206 expression was an independent factor affecting the prognosis of LC patients, as revealed by the Cox regression analysis. In vitro experiments demonstrated that miR-206 overexpression reduced cell multiplication, invasion, and migration and increased cell apoptosis in LC cells. Moreover, SOX9 was a target of miR-206, and miR-206 negatively regulated SOX9 expression. Collectively, miR-206 might be a promising biomarker with diagnostic and prognostic value for LC, and the miR-206/SOX9 axis might be a candidate target for LC therapy.

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          Role of miRNA-Regulated Cancer Stem Cells in the Pathogenesis of Human Malignancies

          Abdul Khan, Eiman I. Ahmed, Noor R. Elareer … (2019)
          Recent biomedical discoveries have revolutionized the concept and understanding of carcinogenesis, a complex and multistep phenomenon which involves accretion of genetic, epigenetic, biochemical, and histological changes, with special reference to MicroRNAs (miRNAs) and cancer stem cells (CSCs). miRNAs are small noncoding molecules known to regulate expression of more than 60% of the human genes, and their aberrant expression has been associated with the pathogenesis of human cancers and the regulation of stemness features of CSCs. CSCs are the small population of cells present in human malignancies well-known for cancer resistance, relapse, tumorigenesis, and poor clinical outcome which compels the development of novel and effective therapeutic protocols for better clinical outcome. Interestingly, the role of miRNAs in maintaining and regulating the functioning of CSCs through targeting various oncogenic signaling pathways, such as Notch, wingless (WNT)/β-Catenin, janus kinases/ signal transducer and activator of transcription (JAK/STAT), phosphatidylinositol 3-kinase/ protein kinase B (PI3/AKT), and nuclear factor kappa-light-chain-enhancer of activated B (NF-kB), is critical and poses a huge challenge to cancer treatment. Based on recent findings, here, we have documented the regulatory action or the underlying mechanisms of how miRNAs affect the signaling pathways attributed to stemness features of CSCs, such as self-renewal, differentiation, epithelial to mesenchymal transition (EMT), metastasis, resistance and recurrence etc., associated with the pathogenesis of various types of human malignancies including colorectal cancer, lung cancer, breast cancer, head and neck cancer, prostate cancer, liver cancer, etc. We also shed light on the fact that the targeted attenuation of deregulated functioning of miRNA related to stemness in human carcinogenesis could be a viable approach for cancer treatment.
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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

            Qing-yong Chen, De-min Jiao, Yu-quan Wu … (2016)
            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.
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              Down-regulation of MiR-206 promotes proliferation and invasion of laryngeal cancer by regulating VEGF expression.

              TianHong Zhang, Kurt Ming-Chao Lin, D. Jin … (2011)
              MicroRNAs (miRNA) are a class of small noncoding RNAs that regulate the expression of their target genes. The aim of the present study was to explore the effects of miR-206 on laryngeal suamous cell carcinoma (LSCC) cells. The expression level of miR-206 was quantified by qRT-PCR in primary LSCC tissues and corresponding adjacent non-neoplastic tissues. MTT, Matrigel invasion assays and flow cytometry methods were used to test the proliferation, invasion and apoptosis of MiR-206 transfection LSCC cells and a mouse model was used to investigate tumorigenesis. MiR-206 was significantly down regulated in the LSCC tissues. Inverse correlation of miR-206 expression was found with the T grade, nodal metastasis and clinical stage of LSCC. Cell proliferation, migration, invasion and tumorigenesis in the LSCC cells were significantly inhibited and apoptotic cells were also increased after miR-206 tansfection. Furthermore, miR-206 transfection down-regulated the expression of vascular endothelial growth factor (VEGF) in the LSCC cells. The loss of miR-206 may play an important role in the progress of LSCC and miR-206 may function as a novel tumor suppressed miRNA.
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                Author and article information

                Contributors
                YunTao Song:
                ORCID: https://orcid.org/0000-0003-4074-9895
                Journal
                Journal ID (nlm-ta): J Healthc Eng
                Journal ID (iso-abbrev): J Healthc Eng
                Journal ID (publisher-id): JHE
                Title: Journal of Healthcare Engineering
                Publisher: Hindawi
                ISSN (Print): 2040-2295
                ISSN (Electronic): 2040-2309
                Publication date Collection: 2021
                Publication date (Electronic): 26 November 2021
                Volume: 2021
                Electronic Location Identifier: 5614861
                Affiliations
                1Department of Otorhinolaryngology, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 45000, China
                2Department of Nursing, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 45000, China
                3Department of Surgery, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 45000, China
                4Dean's Office, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 45000, China
                5Department of Intervention, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 45000, China
                Author notes

                Academic Editor: Yang Gao

                Author information
                https://orcid.org/0000-0003-4074-9895
                Article
                DOI: 10.1155/2021/5614861
                PMC ID: 8642001
                SO-VID: c1f5ff49-dba5-4cba-8c9b-746c52a83004
                Copyright © Copyright © 2021 Yiling Liu et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 26 August 2021
                Date revision received : 22 October 2021
                Date accepted : 28 October 2021
                Funding
                Funded by: Henan Provincial Department of Science and Technology
                Award ID: 212102310141
                Categories
                Subject: Research Article

                Data availability:

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