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      lncRNA H19 acts as a ceRNA to regulate the expression of CTGF by targeting miR- 19b in polycystic ovary syndrome

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          Abstract

          The etiology of polycystic ovary syndrome (PCOS) is complex and the pathogenesis is not fully understood. Some studies have shown that dysregulation of ovarian granulosa cells may be related to abnormal follicles and excessive androgen in women with PCOS. Our team has also confirmed the high expression status of H19 in PCOS patients in the early stage. However, the relationship between H19 and miR- 19b in the development of PCOS is still unknown. Therefore, we used bioinformatics to predict the binding sites of human H19 and miR- 19b, and of miR- 19b and CTGF genes. After the silencing and overexpression of H19, real-time polymerase chain reaction (PCR) was used to detect the expressions of H19, miR- 19b, and CTGF. Western blotting was used to detect CTGF protein. Proliferation of KGN cells after H19 silencing was detected by CCK8. Flow cytometry was used to detect the apoptosis of KGN cells after H19 silencing. After the overexpression of H19, it was found that the expression of miR- 19b gene decreased and the expression of CTGF increased, whereas silencing of H19 did the opposite. In addition, H19 could promote cell proliferation and decrease cell apoptosis. Finally, luciferase reporter assays showed that the 3′-end sequences of lncRNA H19 and CTGF contained the binding site of miR- 19b. In conclusion, our study indicated that lncRNA H19 acted as a ceRNA to bind to miR- 19b via a “sponge” to regulate the effect of CTGF on KGN cells, which may play a vital role in PCOS.

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          Most cited references26

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          In vivo identification of tumor- suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma.

          We recently proposed that competitive endogenous RNAs (ceRNAs) sequester microRNAs to regulate mRNA transcripts containing common microRNA recognition elements (MREs). However, the functional role of ceRNAs in cancer remains unknown. Loss of PTEN, a tumor suppressor regulated by ceRNA activity, frequently occurs in melanoma. Here, we report the discovery of significant enrichment of putative PTEN ceRNAs among genes whose loss accelerates tumorigenesis following Sleeping Beauty insertional mutagenesis in a mouse model of melanoma. We validated several putative PTEN ceRNAs and further characterized one, the ZEB2 transcript. We show that ZEB2 modulates PTEN protein levels in a microRNA-dependent, protein coding-independent manner. Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melanomas and other cancers expressing low PTEN levels. Our study genetically identifies multiple putative microRNA decoys for PTEN, validates ZEB2 mRNA as a bona fide PTEN ceRNA, and demonstrates that abrogated ZEB2 expression cooperates with BRAF(V600E) to promote melanomagenesis. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Influence of metabolic syndrome on female fertility and in vitro fertilization outcomes in PCOS women

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              LncRNA SNHG16 promotes tumor growth of pancreatic cancer by targeting miR-218-5p

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                Author and article information

                Journal
                Braz J Med Biol Res
                Braz J Med Biol Res
                bjmbr
                Brazilian Journal of Medical and Biological Research
                Associação Brasileira de Divulgação Científica
                0100-879X
                1414-431X
                07 October 2020
                2020
                : 53
                : 11
                : e9266
                Affiliations
                [1 ]School of Medicine, Jinan University, Guangzhou, Guangdong Province, China
                [2 ]Guangdong Women and Children Hospital, Guangzhou, Guangdong Province, China
                Author notes
                Correspondence: Xiangcai Wei: < Dxcwei@ 123456163.com >

                *These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-2298-455X
                https://orcid.org/0000-0002-7667-8016
                https://orcid.org/0000-0002-2725-0304
                https://orcid.org/0000-0001-5819-0124
                https://orcid.org/0000-0001-6942-4336
                https://orcid.org/0000-0003-1339-4232
                https://orcid.org/0000-0003-1405-124X
                https://orcid.org/0000-0002-9238-4659
                https://orcid.org/0000-0003-0220-9978
                https://orcid.org/0000-0003-0808-9620
                Article
                00612
                10.1590/1414-431X20209266
                7552896
                33053114
                3cb87c35-317a-4530-8646-ea9bfe39d336

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

                History
                : 26 August 2019
                : 25 June 2020
                Page count
                Figures: 5, Tables: 0, Equations: 0, References: 24
                Categories
                Research Article

                polycystic ovary syndrome,long non-coding rna h19,microrna-19b,ctgf

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