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Updated: Sep 21, 2025

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
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The Interrelationship Between FYN and miR-128/193a-5p/494 in Imatinib Resistance in Prostate Cancer

Sercan Ergün1,2, Oğuzhan Akgün3, Neslihan Taşkurt Hekim1

  • 1Department of Medical Biology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.

Anti-Cancer Agents in Medicinal Chemistry
|June 2, 2022
PubMed
Abstract

Insights

MicroRNAs miR-128/193a-5p/494 may drive imatinib resistance in prostate cancer (PCa) by interacting with the truncated c-KIT (tr-KIT) pathway. Upregulation of FYN in LNCaP cells suggests a mechanism for this resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • C-KIT receptor tyrosine kinase is oncogenic in prostate cancer (PCa).
  • Truncated c-KIT (tr-KIT) protein, lacking extracellular/transmembrane domains, forms complexes with Fyn, Plcγ1, and Sam68.
  • Imatinib inhibits full-length c-KIT but not tr-KIT, which is overexpressed in LNCaP PCa cells.

Purpose of the Study:

  • To investigate the role of specific microRNAs (miRNAs) in imatinib resistance in PCa.
  • To determine if miR-128/193a-5p/494 are associated with imatinib resistance through the tr-KIT pathway.

Main Methods:

  • LNCaP and PC3 PCa cells were treated with imatinib (IC50).
  • RNA was isolated pre- and post-treatment for cDNA conversion.
  • Quantitative PCR (qPCR) analyzed expression of tr-KIT pathway elements and miR-128/193a-5p/494.

Main Results:

  • miR-128/193a-5p/494 were significantly upregulated in LNCaP cells and downregulated in PC3 cells post-imatinib (p<0.05).
  • FYN was significantly upregulated in LNCaP cells post-imatinib (p<0.05), with no change in PC3 cells.

Conclusions:

  • Upregulation of FYN may sequester miR-128/193a-5p/494, reducing their activity in tr-KIT-expressing LNCaP cells.
  • miR-128/193a-5p/494 likely play a crucial role in imatinib resistance via the tr-KIT pathway in PCa.
Keywords:
FYNProstate cancerimatinib resistancemiRNA spongingtruncated KIT (tr-KIT)upregulation

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