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      miR‐451a inhibits cancer growth, epithelial‐mesenchymal transition and induces apoptosis in papillary thyroid cancer by targeting PSMB8

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      Author(s): 1 , 1 ,
      Publication date (Electronic):
      Journal: Journal of Cellular and Molecular Medicine
      Publisher: John Wiley and Sons Inc.
      Keywords: miR‐451a, miRNAs, papillary thyroid cancer, PSMB8

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          Abstract

          Despite the increasing incidence of papillary thyroid cancer in the past decade, the molecular mechanism underlying its progression remains unknown. Several studies have reported down‐regulation of miR‐451a or circular miR‐451a in papillary thyroid cancer cell lines or patients. However, the underlying molecular mechanism remains unknown. In this study, we found that overexpression of miR‐451a could inhibit proliferation, epithelial‐mesenchymal transition and induce apoptosis in papillary thyroid cancer cells. Proteasome subunit beta type‐8 was predicted to be a direct target of miR‐451a and was validated with a luciferase reporter assay. Further functional assays showed that miR‐451a could inhibit thyroid cancer progression by targeting proteasome subunit beta type‐8.

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          Usefulness of Plasma Exosomal MicroRNA-451a as a Noninvasive Biomarker for Early Prediction of Recurrence and Prognosis of Non-Small Cell Lung Cancer

          Rie Kanaoka, Hisae Iinuma, Hitoshi Dejima … (2018)
          Objectives: The aim of this study was to clarify the usefulness of plasma exosomal microRNA-451a (miR-451a) as a novel biomarker for the early prediction of recurrence and prognosis in non-small cell lung cancer (NSCLC) patients after curative resection. Methods: Before surgery, plasma samples were collected and exosomal microRNA (miRNA) levels were evaluated. We first profiled specific exosomal miRNAs related to recurrence in 6 NSCLC patients with stage IA cancer by miRNA microarray. We then validated the usefulness of selected miRNAs as biomarkers using the other 285 NSCLC patients. Results: Plasma exosomal miR-451a showed the highest upregulation in the NSCLC patients with recurrence in the miRNA microarray analysis. A significant positive correlation was demonstrated between exosomal miR-451a levels and NSCLC tissue miR-451a levels. Exosomal miR-451a showed a significant association with lymph node metastasis, vascular invasion, and stage. In stage I, II, or III patients, the overall survival (OS) and disease-free survival (DFS) rates among the high-exosomal-miR-451a patients were significantly worse than those among the low-exosomal-miR-451a patients. In Cox multivariate analysis, exosomal miR-451a showed significance for OS and DFS. Conclusion: Plasma exosomal miR-451a might serve as a reliable biomarker for the prediction of recurrence and prognosis in NSCLC patients with stage I, II, or III cancer.
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            miR-451a is underexpressed and targets AKT/mTOR pathway in papillary thyroid carcinoma

            Emanuela Minna, Paola Romeo, Matteo Dugo … (2016)
            Papillary Thyroid Carcinoma (PTC) is the most frequent thyroid cancer. Although several PTC-specific miRNA profiles have been reported, only few upregulated miRNAs are broadly recognized, while less consistent data are available about downregulated miRNAs. In this study we investigated miRNA deregulation in PTC by miRNA microarray, analysis of a public dataset from The Cancer Genome Atlas (TCGA), literature review and meta-analysis based on a univocal miRNA identifier derived from miRBase v21. A list of 18 miRNAs differentially expressed between PTC and normal thyroid was identified and validated in the TCGA dataset. Furthermore, we compared our signature with miRNA profiles derived from 15 studies selected from literature. Then, to select possibly functionally relevant miRNA, we integrated our miRNA signature with those from two in vitro cell models based on the PTC-driving oncogene RET/PTC1. Through this strategy, we identified commonly deregulated miRNAs, including miR-451a, which emerged also by our meta-analysis as the most frequently reported downregulated miRNA. We showed that lower expression of miR-451a correlates with aggressive clinical-pathological features of PTC as tall cell variant, advanced stage and extrathyroid extension. In addition, we demonstrated that ectopic expression of miR-451a impairs proliferation and migration of two PTC-derived cell lines, reduces the protein levels of its recognized targets MIF, c-MYC and AKT1 and attenuates AKT/mTOR pathway activation. Overall, our study provide both an updated overview of miRNA deregulation in PTC and the first functional evidence that miR-451a exerts tumor suppressor functions in this neoplasia.
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              MiR-451a suppressing BAP31 can inhibit proliferation and increase apoptosis through inducing ER stress in colorectal cancer

              Ke Xu, Bin Han, Yang Bai … (2019)
              The global morbidity and mortality of colorectal cancer (CRC) are ranked the third among gastrointestinal tumors in the world. MiR-451a is associated with several types of cancer, including CRC. However, the roles and mechanisms of miR-451a in CRC have not been elucidated. BAP31 is a predicted target gene of miR-451a in our suppression subtractive hybridization library. Its relationship with miR-451a and function in CRC are unclear. We hypothesized that miR-451a could induce apoptosis through suppressing BAP31 in CRC. Immunohistochemistry and real-time PCR were used to measure BAP31 expressions in CRC tissues and pericarcinous tissues from 57 CRC patients and CRC cell lines. Dual-luciferase reporter assay was used to detect the binding of miR-451a to BAP31. The expression of BAP31 protein in CRC tissues was significantly higher than that in pericarcinous tissues, which was correlated with distant metastasis and advanced clinical stages of CRC patients. The expression of BAP31 was higher in HCT116, HT29, SW620, and DLD cells than that in the normal colonic epithelial cell line NCM460. The expression of BAP31 was absolutely down-regulated when over-expressing miR-451a in HCT116 and SW620 cells compared with control cells. Mir-451a inhibited the expression of BAP31 by binding to its 5’-UTR. Over-expressing miR-451a or silencing BAP31 suppressed the proliferation and apoptosis of CRC cells by increasing the expressions of endoplasmic reticulum stress (ERS)-associated proteins, including GRP78/BIP, BAX, and PERK/elF2α/ATF4/CHOP, which resulted in increased ERS, cytoplasmic calcium ion flowing, and apoptosis of CRC cells. These changes resulting from over-expressing miR-451a were reversed by over-expressing BAP31 with mutated miR-451a-binding sites. Over-expressing miR-451a or silencing BAP31 inhibited tumor growth by inducing ERS. The present study demonstrated that miR-451a can inhibit proliferation and increase apoptosis through inducing ERS by binding to the 5’-UTR of BAP31 in CRC.
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                Author and article information

                Contributors
                Yuejiao Zhao:
                ORCID: https://orcid.org/0000-0002-9329-7047
                zhaoyjlnszl@163.com
                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J. Cell. Mol. Med
                Journal ID (doi): 10.1111/(ISSN)1582-4934
                Journal ID (publisher-id): JCMM
                Title: Journal of Cellular and Molecular Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Electronic): 27 September 2019
                Publication date (Print): December 2019
                Volume: 23
                Issue: 12 ( doiID: 10.1111/jcmm.v23.12 )
                Pages: 8067-8075
                Affiliations
                [ 1 ] Second Ward of Head & Neck Surgery Liaoning Cancer Hospital & Institute (Cancer Hospital of China Medical University) Shenyang China
                Author notes
                [*] [* ] Correspondence

                Yuejiao Zhao, Second Ward of Head & Neck Surgery, Liaoning Province Cancer Hospital & Institute (Cancer Hospital of China Medical University), Shenyang 110004, China.

                Email: zhaoyjlnszl@ 123456163.com

                Author information
                https://orcid.org/0000-0002-9329-7047
                Article
                Publisher ID: JCMM14673
                DOI: 10.1111/jcmm.14673
                PMC ID: 6850967
                PubMed ID: 31559672
                SO-VID: 4be09aaf-e4ba-4169-b8f5-0670205137a7
                Copyright © © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
                License:

                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.

                History
                Date received : 14 May 2019
                Date revision received : 30 July 2019
                Date accepted : 18 August 2019
                Page count
                Figures: 5, Tables: 0, Pages: 9, Words: 3908
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id jcmm14673
                cover-date December 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.7.1 mode:remove_FC converted:12.11.2019

                ScienceOpen disciplines: Molecular medicine
                Keywords: mir‐451a,mirnas,papillary thyroid cancer,psmb8
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: mir‐451a, mirnas, papillary thyroid cancer, psmb8

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