Related Experiment Video

Updated: Oct 2, 2025

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel
06:44

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

Published on: September 8, 2017

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Effects of miR-103a-3p Targeted Regulation of TRIM66 Axis on Docetaxel Resistance and Glycolysis in Prostate Cancer

Qiang Yi1, Junfeng Wei1, Yangzhou Li1

  • 1Department of Urology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, China.

Frontiers in Genetics
|February 25, 2022
PubMed

Insights

This study reveals that low miR-103a-3p and high TRIM66 expression drive prostate cancer (PCa) docetaxel resistance and glycolysis. Restoring miR-103a-3p and inhibiting TRIM66 can overcome resistance and reduce glycolysis in PCa cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Prostate cancer (PCa) remains a significant health concern, with docetaxel (DTX) resistance posing a major therapeutic challenge.
  • Understanding the molecular mechanisms underlying DTX resistance and associated metabolic changes, such as glycolysis, is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the roles of miR-103a-3p and TRIM66 in PCa, focusing on their relationship with DTX resistance and glycolysis.
  • To explore miR-103a-3p's direct targeting of TRIM66 and its impact on PCa cell behavior.

Main Methods:

  • Expression analysis of miR-103a-3p and TRIM66 in normal and PCa cells.
  • Establishment and transfection of DTX-resistant (DR) PCa cells with miR-103a-3p and TRIM66.
  • Assessment of cell viability, proliferation, migration, invasion, and glycolysis using MTT, plate cloning, wound healing, Transwell, and glycolysis assays.

Main Results:

  • PCa cells exhibited low miR-103a-3p and high TRIM66 expression, with a confirmed direct targeting relationship between them.
  • DR PCa cells showed significantly increased DTX resistance, longer doubling times, and altered miR-103a-3p/TRIM66 expression compared to PCa cells.
  • Upregulation of miR-103a-3p and TRIM66 inhibition effectively suppressed proliferation, metastasis, and glycolysis in DR PCa cells.

Conclusions:

  • Downregulated miR-103a-3p and upregulated TRIM66 are associated with PCa progression and DTX resistance.
  • Targeting the miR-103a-3p/TRIM66 axis offers a promising therapeutic strategy to overcome DTX resistance and inhibit glycolysis in PCa.
Keywords:
MiR-103a-3pTRIM66docetaxel resistanceglycolysisprostate cancer

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