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GSDME mediates caspase-3-dependent pyroptosis in gastric cancer

Yubin Wang1, Bo Yin1, Dinuo Li1

  • 1Department of General Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.

Biochemical and Biophysical Research Communications
|November 30, 2017
PubMed

Insights

This study reveals that 5-FU chemotherapy induces pyroptosis, a cell death pathway, in gastric cancer cells by activating GSDME and caspase-3. This finding offers new insights into chemotherapy mechanisms for gastric cancer treatment.

Area of Science:

  • Oncology
  • Cell Biology
  • Immunology

Background:

  • Gastric cancer has a low survival rate, and chemotherapy mechanisms are not fully understood.
  • Pyroptosis, a programmed cell death, is crucial in immunity but its role in cancer is less clear.

Purpose of the Study:

  • To investigate the mechanism of 5-fluorouracil (5-FU) chemotherapy in gastric cancer cells.
  • To explore the role of pyroptosis in 5-FU-induced cell death.

Main Methods:

  • Gastric cancer cell lines (SGC-7901, MKN-45) were treated with 5-FU.
  • Cell viability, LDH release, and Annexin-V/PI staining were assessed.
  • GSDME and GSDMD cleavage, and caspase-3 activity were analyzed.
  • GSDME knockout using CRISPR-Cas9 was performed.

Main Results:

  • 5-FU significantly decreased cell viability and increased markers of cell death.
  • Evidence of pyroptosis, including membrane blebbing and GSDME cleavage, was observed.
  • Caspase-3 inhibition or GSDME knockout blocked pyroptosis, switching cell death to apoptosis.

Conclusions:

  • Gastric cancer cells undergo pyroptosis in response to 5-FU chemotherapy.
  • The GSDME-caspase-3 pathway is critical for 5-FU-induced pyroptosis in gastric cancer.
  • This study elucidates a novel mechanism of chemotherapy-induced cell death in gastric cancer.
Keywords:
Caspase-3GSDMEGastric cancerPyroptosis

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