Endoplasmic Reticulum Stress-Induced JNK Activation Is a Critical Event Leading to Mitochondria-Mediated Cell Death Caused by β-Lapachone Treatment
2011

How β-Lapachone Causes Cancer Cell Death

publication Evidence: moderate

Author Information

Author(s): Lee Hyemi, Park Moon-Taek, Choi Bo-Hwa, Oh Eun-Taex, Song Min-Jeong, Lee Jeonghun, Kim Chulhee, Lim Byung Uk, Park Heon Joo

Primary Institution: Inha University, Incheon, Republic of Korea

Hypothesis

Does β-lapachone induce apoptosis in cancer cells through specific signaling pathways?

Conclusion

β-lapachone triggers endoplasmic reticulum stress, leading to JNK activation and mitochondria-mediated apoptosis in cancer cells.

Supporting Evidence

  • β-lapachone induces apoptosis in an NQO1-dependent manner.
  • JNK activation is required for the apoptotic cell death caused by β-lapachone.
  • ER stress is necessary for JNK activation in response to β-lapachone treatment.
  • Cleaved Bax translocates to mitochondria, contributing to cell death.
  • Pharmacological inhibitors of JNK reduce β-lapachone-induced cell death.

Takeaway

This study shows that a natural compound called β-lapachone can make cancer cells die by stressing them out and messing with their energy factories, called mitochondria.

Methodology

The study used NQO1-negative and NQO1-overexpressing MDA-MB-231 cells to investigate the effects of β-lapachone on apoptosis and related signaling pathways.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0021533

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