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Synergy between arsenic trioxide and JQ1 on autophagy in pancreatic cancer

Congling Xu1,2, Xinrui Wang1, Yu Zhou3

  • 1State Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital Affiliated to School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

Oncogene
|August 18, 2019
PubMed

Insights

This study reveals a novel pancreatic cancer treatment combining arsenic trioxide (ATO) and BET inhibitor JQ1. This combination synergistically induces apoptosis by modulating autophagy and ER stress, offering a promising strategy for this deadly malignancy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Pancreatic cancer is a highly lethal malignancy with limited effective treatment options.
  • Understanding the molecular mechanisms of cell death is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the synergistic effect of arsenic trioxide (ATO) and JQ1 in treating pancreatic cancer.
  • To elucidate the role of autophagy, ER stress, and NRF2 in ATO-induced apoptosis.

Main Methods:

  • Combination treatment of pancreatic cancer cells with ATO and JQ1.
  • Genomic and biochemical analyses to study autophagy, ER stress, and NRF2.
  • NRF2 depletion experiments to assess its role in treatment sensitivity.

Main Results:

  • ATO and JQ1 synergistically induce apoptosis in pancreatic cancer cells.
  • The combination modulates autophagy and ER stress, crucial pathways in ATO-induced cell death.
  • NRF2 plays a key role in cell survival, and its depletion enhances sensitivity to ATO.

Conclusions:

  • The combination of ATO and JQ1 represents a potential new therapeutic strategy for pancreatic cancer.
  • Targeting the interplay between ER stress, autophagy, and NRF2 could overcome treatment resistance.

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