Related Experiment Video

Updated: May 12, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
04:01

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

792

JS-K induces ferroptosis in renal carcinoma cells by regulating the c-Myc-GSTP1 Axis

Yuwan Zhao1, LuGang Zhu1, Xinghua Lin1

  • 1Laboratory of Urology, Affiliated Hospital of Guangdong Medical University, 57 Renmin Street South, Zhanjiang, 524001, Guangdong, China.

Scientific Reports
|May 9, 2025
PubMed

Insights

JS-K triggers ferroptosis, a cell death pathway, in renal cell carcinoma (RCC) by depleting glutathione. This mechanism inhibits tumor growth, offering a potential new strategy for RCC treatment.

Area of Science:

  • Biochemistry
  • Oncology
  • Cell Biology

Background:

  • Ferroptosis, a lipid peroxidation-driven cell death, is implicated in cancer.
  • JS-K, a nitric oxide precursor, exhibits anti-tumor properties.
  • The role of ferroptosis in JS-K's anti-cancer effects remains unclear.

Purpose of the Study:

  • To investigate if JS-K induces ferroptosis in renal cell carcinoma (RCC).
  • To elucidate the molecular mechanisms underlying JS-K-induced ferroptosis in RCC.
  • To evaluate the anti-tumor efficacy of JS-K in a preclinical RCC model.

Main Methods:

  • In vitro cytotoxicity assays on RCC and normal renal cells.
  • Measurement of intracellular ferrous ions, glutathione (GSH), lipid peroxides, and malondialdehyde (MDA).
  • Western blotting for protein expression analysis and in vivo xenograft studies.

Main Results:

  • JS-K selectively inhibited RCC cell growth, inducing ferroptosis by reducing GSH and increasing lipid peroxidation.
  • JS-K downregulated GSTP1 via inhibition of the c-Myc transcription factor.
  • JS-K demonstrated significant anti-tumor activity in a mouse model by inducing ferroptosis.

Conclusions:

  • JS-K induces ferroptosis in RCC cells through glutathione depletion via the c-Myc-GSTP1 pathway.
  • JS-K exhibits potent anti-tumor effects in RCC, mediated by ferroptosis.
  • JS-K represents a promising therapeutic agent for renal cell carcinoma.
Keywords:
FerroptosisGSTP1JS-KRenal cell carcinomac-Myc

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