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Ferroptosis is a lysosomal cell death process.

Huan Gao1, Yuansong Bai1, Yuanyuan Jia1

  • 1Department of Oncology and Hematology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130021, China.

Biochemical and Biophysical Research Communications
|July 23, 2018
PubMed
Summary

Signal transducer and activator of transcription 3 (STAT3) promotes ferroptosis, a cell death pathway crucial in pancreatic cancer. STAT3 activation, via MAPK/ERK, upregulates cathepsin B, driving lysosomal cell death in ferroptosis.

Keywords:
AutophagyCathepsinFerroptosisLysosomal cell deathSTAT3

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Area of Science:

  • Cell Biology
  • Oncology
  • Biochemistry

Background:

  • Ferroptosis, a regulated cell death, involves iron accumulation and lipid peroxidation.
  • Dysregulation of ferroptosis is implicated in various human diseases.
  • The precise mechanisms governing ferroptosis remain incompletely understood.

Purpose of the Study:

  • To investigate the role of Signal Transducer and Activator of Transcription 3 (STAT3) in regulating ferroptosis.
  • To elucidate the molecular pathways involved in STAT3-mediated ferroptosis in pancreatic ductal adenocarcinoma (PDAC).

Main Methods:

  • Utilized human PDAC cell lines.
  • Investigated STAT3 activation through MAPK/ERK pathway.
  • Employed pharmacological inhibitors (cryptotanshinone, S3I-201, CA-074Me, bafilomycin A1) and genetic silencing (siRNA) of STAT3 and cathepsin B.
  • Assessed erastin-induced ferroptosis.

Main Results:

  • STAT3 acts as a positive regulator of ferroptosis in PDAC cells.
  • STAT3 activation during erastin-induced ferroptosis requires MAPK/ERK pathway activation.
  • STAT3 inhibition (pharmacological or genetic) significantly blocks erastin-induced ferroptosis.
  • STAT3-dependent cathepsin B expression is essential for ferroptosis.
  • Inhibiting lysosomal function (cathepsin activity or vacuolar H+-ATPase) limits ferroptosis.

Conclusions:

  • STAT3 is a key positive regulator of ferroptosis in pancreatic cancer.
  • Ferroptosis involves lysosome-dependent cell death mechanisms.
  • Targeting STAT3 or lysosomal pathways may offer therapeutic strategies for PDAC.