Mendeley | Further Information

{"title"=>"MiR-375 is epigenetically downregulated by HPV-16 E6 mediated DNMT1 upregulation and modulates EMT of cervical cancer cells by suppressing IncRNA MALAT1", "type"=>"journal", "authors"=>[{"first_name"=>"Shikai", "last_name"=>"Liu", "scopus_author_id"=>"56306257500"}, {"first_name"=>"Lili", "last_name"=>"Song", "scopus_author_id"=>"56565864500"}, {"first_name"=>"Hairong", "last_name"=>"Yao", "scopus_author_id"=>"57190031921"}, {"first_name"=>"Liang", "last_name"=>"Zhang", "scopus_author_id"=>"56305617100"}, {"first_name"=>"Dongkui", "last_name"=>"Xu", "scopus_author_id"=>"57190034316"}, {"first_name"=>"Fangyuan", "last_name"=>"Gao", "scopus_author_id"=>"56565858100"}, {"first_name"=>"Qian", "last_name"=>"Li", "scopus_author_id"=>"57199178730"}], "year"=>2016, "source"=>"PLoS ONE", "identifiers"=>{"scopus"=>"2-s2.0-84992176867", "sgr"=>"84992176867", "doi"=>"10.1371/journal.pone.0163460", "pui"=>"612774203", "pmid"=>"27658300", "issn"=>"19326203"}, "id"=>"40019cd9-ccd1-34d3-858f-55a97e0500cd", "abstract"=>"Epigenetic modulation is an important mechanism of miRNA dysregulation in cervical cancer. In this study, we firstly studied how this mechanism contributes to miR-375 downregulation in cervical cancer cells. Then, we further studied the association between miR-375 and MALAT1 (metastasis associated lung adenocarcinoma transcript 1) in epithelial mesenchymal transition (EMT) of the cancer cells. HPV-16 positive SiHa and CaSki cells were used as in vitro model. Our data showed that HPV-16 E6 positively modulated DNMT1 expression in both SiHa and CaSki cells. Knockdown of DNMT1 partly restored miR-375 levels in the cells. The following methylation-specific PCR (MSP) assay and qRT-PCR analysis showed that methylation was common in the promoter region of miR-375 in both SiHa and CaSki cells and demethylation partly restored miR-375 levels in the cells. Therefore, we infer that miR-375 is downregulated partly due to promoter hypermethylation mediated by DNMT1 in HPV-16 positive cervical cancer cells. Our bioinformatics analysis showed that MALAT1 has three putative binding sites with miR-375 and the following dual luciferase assay confirmed two of them. QRT-PCR analysis showed that miR-375 overexpression significantly reduced MALAT1 expression, while MALAT1 overexpression reversely suppressed miR-375 levels. Therefore, we infer that there is a reciprocal regulation between miR-375 and MALAT1 in the cells. In SiHa cells, miR-375 overexpression or MALAT1 siRNA partly restored E-cadherin expression, significantly reduced N-cadherin and also reduced invasion capacity of SiHa cells. Therefore, these results suggest that miR-375 and MALAT1 form a functional axis modulating EMT in cervical cancer.", "link"=>"http://www.mendeley.com/research/mir375-epigenetically-downregulated-hpv16-e6-mediated-dnmt1-upregulation-modulates-emt-cervical-canc", "reader_count"=>51, "reader_count_by_academic_status"=>{"Unspecified"=>5, "Researcher"=>2, "Student > Ph. D. Student"=>2, "Student > Postgraduate"=>26, "Student > Master"=>5, "Other"=>2, "Student > Bachelor"=>9}, "reader_count_by_user_role"=>{"Unspecified"=>5, "Researcher"=>2, "Student > Ph. D. Student"=>2, "Student > Postgraduate"=>26, "Student > Master"=>5, "Other"=>2, "Student > Bachelor"=>9}, "reader_count_by_subject_area"=>{"Unspecified"=>5, "Biochemistry, Genetics and Molecular Biology"=>32, "Medicine and Dentistry"=>1, "Agricultural and Biological Sciences"=>12, "Neuroscience"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>1}, "Neuroscience"=>{"Neuroscience"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>12}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>32}, "Unspecified"=>{"Unspecified"=>5}}, "group_count"=>3}

CrossRef

• http://doi.org/10.1002/jcp.26759
• http://doi.org/10.3390/cancers10120493
• http://doi.org/10.1186/s12885-018-5206-8
• http://doi.org/10.3389/fonc.2019.00847
• http://doi.org/10.1186/s13148-017-0424-5
• http://doi.org/10.3892/or.2017.5905
• http://doi.org/10.1371/journal.pone.0224167
• http://doi.org/10.1186/s12943-017-0671-2
• http://doi.org/10.3389/fonc.2018.00111
• http://doi.org/10.1016/j.biopha.2019.108944
• http://doi.org/10.1186/s13148-018-0509-9
• http://doi.org/10.21294/1814-4861-2019-18-2-92-101
• http://doi.org/10.1111/cpr.12461
• http://doi.org/10.1038/s41598-019-40094-8
• http://doi.org/10.1177/1073274818803942
• http://doi.org/10.1016/j.cyto.2017.04.001
• http://doi.org/10.1186/s13045-018-0606-4

Scopus | Further Information

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