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A reactive oxygen species activation mechanism contributes to JS-K-induced apoptosis in human bladder cancer cells

Mingning Qiu1, Lieqian Chen1, Guobin Tan1

  • 1Laboratory of Urology, Guangdong Medical University, Zhanjiang 524001, China.

Scientific Reports
|October 14, 2015
PubMed

Insights

The compound JS-K suppresses bladder cancer cell proliferation and induces apoptosis by increasing reactive oxygen species (ROS). JS-K also enhances chemotherapy effectiveness, offering a potential new treatment strategy.

Area of Science:

  • Oncology
  • Biochemistry
  • Cell Biology

Background:

  • Reactive oxygen species (ROS) and cellular oxidant stress are key regulators in cancer cell biology.
  • Altered redox status, driven by ROS, increases cancer cell susceptibility to oxidative stress.

Purpose of the Study:

  • To investigate the effects of JS-K on bladder cancer cell proliferation and apoptosis.
  • To explore the underlying ROS-related mechanisms of JS-K action.

Main Methods:

  • JS-K treatment of bladder cancer cells at varying concentrations and durations.
  • Assessment of cell proliferation, apoptosis markers, and ROS levels.
  • Investigation using antioxidants (NAC) and prooxidants (GSSG).

Main Results:

  • JS-K inhibited bladder cancer cell proliferation and induced apoptosis and ROS accumulation in a dose- and time-dependent manner.
  • JS-K increased the expression of apoptosis-related proteins.
  • Antioxidant NAC reversed JS-K-induced apoptosis, while GSSG exacerbated it.
  • JS-K enhanced doxorubicin chemo-sensitivity.

Conclusions:

  • JS-K-released nitric oxide (NO) induces bladder cancer cell apoptosis via increased ROS levels.
  • Oxidized nitrites from JS-K-released NO contribute to sustained apoptosis.
  • JS-K shows potential as a therapeutic agent for bladder cancer, possibly in combination therapy.

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