ArticleFree radical biology & medicine2012
Capsazepine, a TRPV1 antagonist, sensitizes colorectal cancer cells to apoptosis by TRAIL through ROS-JNK-CHOP-mediated upregulation of death receptors.
Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- The Impact of TRPV1 on Cancer Pathogenesis and Therapy: A Systematic Review.International journal of biological sciences · 2021Pooled it
- Capsaicin Receptor TRPV1 Delays Aortic Aging in Atherosclerotic Mice by Inhibiting the ISG15-p53 Pathway.Journal of cellular and molecular medicine · 2026Article
- Natural and Synthetic Capsaicin Analogues: A Comprehensive Review of Biological Effects and Synthetic Pathways.Current medicinal chemistry · 2025Review
- Cell-free adipose tissue extracts as a novel treatment for rosacea by downregulating TRPV1.Scientific reports · 2024Article
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- TRPV1 inhibition suppresses non-small cell lung cancer progression by inhibiting tumour growth and enhancing the immune response.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Anti-cancer activity and mechanism of flurbiprofen organoselenium compound RY-1-92 in non-small cell lung cancer.RSC medicinal chemistry · 2024Article
- TRP Channels in Tumoral Processes Mediated by Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2023Review
- Unraveling the Complexity of Regulated Cell Death in Esophageal Cancer: from Underlying Mechanisms to Targeted Therapeutics.International journal of biological sciences · 2023Review
- New Frontiers on ER Stress Modulation: Are TRP Channels the Leading Actors?International journal of molecular sciences · 2022Review
- Chloroquine regulates the proliferation and apoptosis of palate development on mice embryo by activating P53 through blocking autophagy in vitro.In vitro cellular & developmental biology. Animal · 2022Article
- Hydrosols fromPlants (Basel, Switzerland) · 2022Article
- Transient receptor potential (TRP) channels in human colorectal cancer: evidence and perspectives.Histology and histopathology · 2021Review
- Ascorbate-induced oxidative stress mediates TRP channel activation and cytotoxicity in human etoposide-sensitive and -resistant retinoblastoma cells.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- How Dysregulated Ion Channels and Transporters Take a Hand in Esophageal, Liver, and Colorectal Cancer.Reviews of physiology, biochemistry and pharmacology · 2021Review
- The Effects of Capsaicin on Gastrointestinal Cancers.Molecules (Basel, Switzerland) · 2020Review
- The Role of Oxidative Stress and Its Counteractive Utility in Colorectal Cancer (CRC).Cancers · 2020Review
- Non-Thermal Plasma Couples Oxidative Stress to TRAIL Sensitization through DR5 Upregulation.International journal of molecular sciences · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
A major problem in clinical trials of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as cancer therapy is the development of resistance to TRAIL. Therefore, agents that can overcome TRAIL resistance have great therapeutic potential. In this study, we evaluated capsazepine, a TRPV1 antagonist, for its ability to sensitize human colon cancer cells to TRAIL-induced apoptosis. Capsazepine potentiated the effect of TRAIL, as shown by its effect on intracellular esterase activity; activation of caspase-8,-9, and -3; and colony-formation assay. Capsazepine induced death receptors (DRs) DR5 and DR4, but not decoy receptors, at the transcriptional level and in a non-cell-type-specific manner. DR induction was dependent on CCAAT/enhancer-binding protein homologous protein (CHOP), as shown by (a) the induction of CHOP by capsazepine and (b) the abolition of DR- and potentiation of TRAIL-induced apoptosis by CHOP gene silencing. CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine's ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL. Capsazepine's effects appeared to be mediated via JNK, as shown by capsazepine's ability to induce JNK and by the suppression of both CHOP and DR5 activation by inhibition of JNK. Furthermore, ROS sequestration abrogated the activation of JNK. Finally, capsazepine downregulated the expression of various antiapoptotic proteins (e.g., cFLIP and survivin) and increased the expression of proapoptotic proteins (e.g., Bax and p53). Together, our results indicate that capsazepine potentiates the apoptotic effects of TRAIL through downregulation of cell survival proteins and upregulation of death receptors via the ROS-JNK-CHOP-mediated pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.