Paper
11 February 2010 Involvement of ASK1 activation in apoptosis induced by NPe6-PDT
Lei Liu, Zhen-zhen Zhang, Zhigang Zhang
Author Affiliations +
Proceedings Volume 7565, Biophotonics and Immune Responses V; 75650L (2010) https://doi.org/10.1117/12.840472
Event: SPIE BiOS, 2010, San Francisco, California, United States
Abstract
Photodynamic therapy (PDT) employing photosensiter N-aspartyl chlorin e6 (NPe6) can induce lysosome disruption and initiate apoptotic pathway. Apoptosis signal-regulating kinase (ASK1) is an important regulator of apoptosis in response to various stresses, such as reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, lipopolysaccharide (LPS) and calcium influx. In this study, we investigated the molecular mechanisms of apoptosis induced by NPe6-PDT in ASTC-a-1 cells. The results showed that the activities of ASK1 increased in response to NPe6-PDT. Over-expression of wild-type or activated mutant of ASK1 could obviously decrease cell viability and increase cell death; while inhibition of ASK1 significantly decreased cell apoptosis. These results suggested that ASK1 plays an important role in apoptosis induced by NPe6-PDT.
© (2010) COPYRIGHT Society of Photo-Optical Instrumentation Engineers (SPIE). Downloading of the abstract is permitted for personal use only.
Lei Liu, Zhen-zhen Zhang, and Zhigang Zhang "Involvement of ASK1 activation in apoptosis induced by NPe6-PDT", Proc. SPIE 7565, Biophotonics and Immune Responses V, 75650L (11 February 2010); https://doi.org/10.1117/12.840472
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KEYWORDS
Cell death

Photodynamic therapy

Molecular mechanisms

Oxygen

Proteins

Calcium

Tumors

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