Please use this identifier to cite or link to this item: https://doi.org/10.3390/molecules24050995
Title: Pleiotropic pharmacological actions of capsazepine, a synthetic analogue of capsaicin, against various cancers and inflammatory diseases
Authors: Yang, M.H.
Jung, S.H.
Sethi, G. 
Ahn, K.S.
Keywords: Cancer
Capsazepine
Inflammatory diseases
ROS
TRPV1
Issue Date: 2019
Publisher: MDPI AG
Citation: Yang, M.H., Jung, S.H., Sethi, G., Ahn, K.S. (2019). Pleiotropic pharmacological actions of capsazepine, a synthetic analogue of capsaicin, against various cancers and inflammatory diseases. Molecules 24 (5) : 995. ScholarBank@NUS Repository. https://doi.org/10.3390/molecules24050995
Rights: Attribution 4.0 International
Abstract: Capsazepine is a synthetic analogue of capsaicin that can function as an antagonist of TRPV1. Capsazepine can exhibit diverse effects on cancer (prostate cancer, breast cancer, colorectal cancer, oral cancer, and osteosarcoma) growth and survival, and can be therapeutically used against other major disorders such as colitis, pancreatitis, malaria, and epilepsy. Capsazepine has been reported to exhibit pleiotropic anti-cancer effects against numerous tumor cell lines. Capsazepine can modulate Janus activated kinase (JAK)/signal transducer and activator of the transcription (STAT) pathway, intracellular Ca2+ concentration, and reactive oxygen species (ROS)-JNK-CCAAT/enhancer-binding protein homologous protein (CHOP) pathways. It can inhibit cell proliferation, metastasis, and induce apoptosis. Moreover, capsazepine can exert anti-inflammatory effects through the downregulation of lipopolysaccharide (LPS)-induced nuclear transcription factor-kappa B (NF-?B), as well as the blockage of activation of both transient receptor potential cation channel subfamily V member 1 (TRPV1) and transient receptor potential cation channel, subfamily A, and member 1 (TRPA1). This review briefly summarizes the diverse pharmacological actions of capsazepine against various cancers and inflammatory conditions. © 2019 by the authors.
Source Title: Molecules
URI: https://scholarbank.nus.edu.sg/handle/10635/210059
ISSN: 1420-3049
DOI: 10.3390/molecules24050995
Rights: Attribution 4.0 International
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