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      miR‐145 promotes miR‐133b expression through c‐myc and DNMT3A‐mediated methylation in ovarian cancer cells

      1 , 2 , 3 , 3 , 3 , 3
      Journal of Cellular Physiology
      Wiley

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          Abstract

          Ovarian cancer presents as malignant tumors in the female reproductive system with high mortality. MicroRNAs are involved in the progression of ovarian cancer; however, the regulatory relationship among miRs remains unclear. In our study, we verified that both miR-145 and miR-133b messenger RNA (mRNA) levels in ovarian cancer tissues were lower than in normal ovarian tissues, and their mRNA level in serum of patients with ovarian cancer was reduced. We demonstrated miR-145 targeted c-myc, and c-myc interacted physically with DNMT3A in ovarian cancer cells. We confirmed that c-myc recruited DNMT3A to the miR-133b promoter. miR-133b overexpression also inhibited target gene PKM2 expression along with the Warburg effect. Our results indicate that miR-145 inhibited the Warburg effect through miR-133b/PKM2 pathways, which may improve approaches to ovarian cancer diagnosis and treatment.

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          Author and article information

          Contributors
          Journal
          Journal of Cellular Physiology
          J Cell Physiol
          Wiley
          0021-9541
          1097-4652
          October 29 2019
          May 2020
          October 14 2019
          May 2020
          : 235
          : 5
          : 4291-4301
          Affiliations
          [1 ]Department of PathologyThe First Affiliated Hospital of Xi'an Jiaotong UniversityXi'an China
          [2 ]Department of Structural Heart DiseaseThe First Affiliated Hospital of Xi'an Jiaotong UniversityXi'an China
          [3 ]Department of Gynecology and ObstetricsThe First Affiliated Hospital of Xi'an Jiaotong UniversityXi'an China
          Article
          10.1002/jcp.29306
          31612498
          5c71cec1-6947-4fa4-8abb-706d725ea2d5
          © 2020

          http://onlinelibrary.wiley.com/termsAndConditions#vor

          http://doi.wiley.com/10.1002/tdm_license_1.1

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