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A newly synthesized compound induces apoptosis in prostate cancer cells by targeting mitochondrial dysfunction and

Neslihan Meriç1, Ezgi Kar2, Fatih Kar3

  • 1Department of Molecular Biology and Genetics, Faculty of Engineering and Natural Sciences, Kütahya Health Sciences University, Kütahya, Turkey.

Biochemical and Biophysical Research Communications
|November 19, 2025
PubMed

Insights

A novel thiazole derivative effectively reduced prostate cancer cell viability and induced apoptosis. The compound selectively targeted cancer cells, modulating inflammatory signaling and supporting its therapeutic potential in oncology.

Area of Science:

  • Oncology
  • Medicinal Chemistry
  • Molecular Biology

Background:

  • Thiazole derivatives show promise as anticancer agents.
  • Prostate cancer remains a significant health concern, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To evaluate the cytotoxic and mechanistic effects of a novel thiazole compound on PC-3 prostate cancer cells.
  • To investigate the compound's impact on apoptosis, gene expression, and inflammatory markers.

Main Methods:

  • Cell viability assays (MTT or similar).
  • Annexin V/PI staining for apoptosis detection.
  • JC-1 assay for mitochondrial membrane potential.
  • RT-qPCR for gene expression analysis (PSA, c-MYC, TP53).
  • ELISA for protein quantification (Caspase-3, Cytochrome-c, GPX4, SEMA3A).
  • Cytokine analysis (TNF-α, IL-6, IL-10).

Main Results:

  • The thiazole compound significantly decreased PC-3 cell viability and induced apoptosis in a dose-dependent manner.
  • Mitochondrial membrane depolarization and activation of intrinsic apoptosis pathways were observed.
  • Downregulation of PSA and c-MYC, with a mild increase in TP53, was noted.
  • Elevated Caspase-3 and modulated Cytochrome-c supported apoptosis.
  • Increased TNF-α levels suggest modulation of inflammatory signaling.

Conclusions:

  • The synthesized thiazole derivative exhibits selective cytotoxicity against prostate cancer cells.
  • The compound induces cell death via mitochondria-mediated apoptosis.
  • Modulation of inflammatory signaling pathways is implicated in its anticancer effects.
Keywords:
4-MethylthiazoleApoptosisCell cycleInflammatory signalingMitochondrial dysfunctionPC-3 cellsSEMA3A

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