1. Academic Validation
  2. MiR-138-5p inhibits prostate cancer cell proliferation and chemoresistance by targeting APOBEC3B

MiR-138-5p inhibits prostate cancer cell proliferation and chemoresistance by targeting APOBEC3B

  • Transl Oncol. 2023 Jun 24;35:101723. doi: 10.1016/j.tranon.2023.101723.
Lina Liu 1 Yan Zhang 1 Xi Hu 1 Hui Zhang 1 Chenyang Jiang 1 Yan Guo 1 Shundong Cang 2
Affiliations

Affiliations

  • 1 Department of Oncology, Henan Provincial International Coalition Laboratory of Oncology Precision Treatment, Henan Provincial Academician Workstation of Non-coding RNA Translational Research, Henan Provincial People's Hospital, Henan University People's Hospital and Zhengzhou University People's Hospital, Zhengzhou, 450003, Henan, China.
  • 2 Department of Oncology, Henan Provincial International Coalition Laboratory of Oncology Precision Treatment, Henan Provincial Academician Workstation of Non-coding RNA Translational Research, Henan Provincial People's Hospital, Henan University People's Hospital and Zhengzhou University People's Hospital, Zhengzhou, 450003, Henan, China. Electronic address: shundongcang@zzu.edu.cn.
Abstract

Docetaxel is one of the most commonly used drugs in prostate Cancer (PCa) chemotherapy, but its therapeutic effect in PCa is usually limited due to its drug resistance. APOBEC3B is a DNA cytosine deaminase that can alter biological processes, including chemoresistance. APOBEC3B is upregulated in various cancers. However, the biological function and underlying regulation of APOBEC3B in PCa remain unclear. In this study, we explored the role of APOBEC3B in PCa chemoresistance and the molecular mechanism of its dysregulated expression. Our results revealed that APOBEC3B was upregulated in PCa docetaxel-resistant cells, while its knockdown significantly repressed cell proliferation and docetaxel resistance of PCa cells. Bioinformatics and luciferase report analysis showed that miR-138-5p targeted APOBEC3B. In addition, miR-138-5p overexpression impeded cell proliferation and docetaxel resistance in PCa, while miR-138-5p inhibitors reversed this process. Further studies showed that upregulation of APOBEC3B expression in docetaxel-resistant cells overexpressing miR-138-5p could desensitize PCa cells to docetaxel treatment. Taken together, miR-138-5p regulates PCa cell proliferation and chemoresistance by targeting the 3'-UTR of APOBEC3B, which may provide novel insights and therapeutic targets for the treatment of PCa.

Keywords

APOBEC3B; Chemoresistance; Docetaxel; Prostate cancer; miR-138–5p.

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