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Curcuminoid B63 induces ROS-mediated paraptosis-like cell death by targeting TrxR1 in gastric cells

Xi Chen1, Xiaoming Chen2, Xi Zhang3

  • 1Chemical Biology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China; Affiliated Yueqing Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325600, China.

Redox Biology
|December 28, 2018
PubMed

Insights

A novel curcumin analog, B63, effectively targets gastric cancer cells by inducing oxidative stress and caspase-independent paraptosis. This approach offers a promising new strategy against chemotherapy-resistant gastric cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Gastric cancer remains a leading cause of cancer mortality worldwide.
  • Chemotherapy improves survival but faces challenges due to drug resistance.
  • Caspase-independent cell death, such as paraptosis, is an emerging therapeutic target.

Purpose of the Study:

  • To evaluate the anti-cancer effects and underlying mechanisms of curcumin analog B63 in gastric cancer cells.
  • To investigate B63's potential to overcome chemoresistance.
  • To explore B63's role in inducing paraptosis.

Main Methods:

  • In vitro studies on gastric cancer cell lines, including 5-fluorouracil-resistant cells.
  • Assessment of B63's effect on thioredoxin reductase 1 (TrxR1) and reactive oxygen species (ROS) levels.
  • Analysis of endoplasmic reticulum (ER) stress, MAPK activation, and cell death pathways.
  • In vivo studies using gastric cancer xenograft models.

Main Results:

  • B63 targets TrxR1, leading to increased cellular ROS and induction of caspase-independent paraptosis.
  • B63-induced paraptosis is mediated by ROS-dependent ER stress and MAPK activation.
  • Overexpression of TrxR1 or ROS suppression abrogated B63-induced paraptosis.
  • B63 demonstrated efficacy against 5-fluorouracil-resistant cells and reduced tumor growth in vivo, associated with increased ROS and paraptosis.

Conclusions:

  • B63 represents a novel therapeutic agent for gastric cancer, inducing cell death via TrxR1-mediated oxidative stress and paraptosis.
  • This mechanism offers a potential strategy to overcome chemoresistance in gastric cancer.
  • B63 warrants further investigation as a new treatment modality for gastric cancer.
Keywords:
Drug resistanceER stressGastric cancerOxidative stressParaptosisTrxR1

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