2. Academic Validation
  3. Cantharidic acid induces apoptosis in human nasopharyngeal carcinoma cells through p38-mediated upregulation of caspase activation

Cantharidic acid induces apoptosis in human nasopharyngeal carcinoma cells through p38-mediated upregulation of caspase activation

  • Environ Toxicol. 2020 May;35(5):619-627. doi: 10.1002/tox.22897.
Yi-Ching Chen 1,  Pei-Ni Chen 2,  Chiao-Wen Lin 3 4,  Wei-En Yang 1 5,  Yu-Ting Ho 5,  Shun-Fa Yang 1 5,  Chun-Yi Chuang 6 7
Affiliations

Affiliations

  • 1 Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
  • 2 Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
  • 3 Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan.
  • 4 Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan.
  • 5 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
  • 6 School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
  • 7 Department of Otolaryngology, Chung Shan Medical University Hospital, Taichung, Taiwan.
PMID: 31916385 DOI: 10.1002/tox.22897
Abstract

Cantharidic acid (CA) is the hydrolysis product of the acid anhydride cantharidin, which is a natural toxin secreted by several species of blister beetles. Several studies have indicated that as an inhibitor of protein Phosphatase 2 (PP2A), CA induces Apoptosis in various human Cancer cells. However, the effect of CA on human nasopharyngeal carcinoma (NPC) cells and the underlying pathways have not been addressed. In our current study, we tested the hypothesis that CA treatment reduces the viability of human NPC cells (HONE-1, NPC-39, and NPC-BM) by inducing Apoptosis. Results indicated that CA markedly reduced cell viability, which was revealed by the upregulation of Caspase activation in extrinsic and intrinsic Apoptosis pathways as well as the upregulation of extracellular-signal-regulated kinase 1/2 (ERK1/2), p38, and c-Jun N-terminal kinase 1/2 (JNK1/2) pathways. Coadministration of a p38 inhibitor (SB203580) with CA abolished the activation of Caspase proteins. These findings indicated that CA treatment leads to Apoptosis in human NPC cells through the upregulation of Caspase activation, mediated particularly by the p38 pathway. Hence, CA is a promising therapeutic agent for human NPC.

Keywords

MAPK; apoptosis; cantharidic acid; caspase; nasopharyngeal carcinoma.

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