ArticleMolecules (Basel, Switzerland)2014
Camalexin-induced apoptosis in prostate cancer cells involves alterations of expression and activity of lysosomal protease cathepsin D.
Article in Molecules (Basel, Switzerland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- An Efficient Method for the Synthesis and In Silico Study of Novel Oxy-Camalexins.Molecules (Basel, Switzerland) · 2025Article
- Article
- Human Cytomegalovirus Protein pUL38 Prevents Premature Cell Death by Binding to Ubiquitin-Specific Protease 24 and Regulating Iron Metabolism.Journal of virology · 2018Article
- Epistructured catechins, EGCG and EC facilitate apoptosis induction through targeting de novo lipogenesis pathway in HepG2 cells.Cancer cell international · 2018Article
- Cathepsin D protects renal tubular cells from damage induced by high glucose independent of its enzymatic activity.American journal of translational research · 2017Article
- Antiproliferative Effect of Indole Phytoalexins.Molecules (Basel, Switzerland) · 2016Review
- Anticancer effect of deoxypodophyllotoxin induces apoptosis of human prostate cancer cells.Oncology letters · 2016Article
- Deciphering the role of phytoalexins in plant-microorganism interactions and human health.Molecules (Basel, Switzerland) · 2014Review
- ROS-dependent antiproliferative effect of brassinin derivative homobrassinin in human colorectal cancer Caco2 cells.Molecules (Basel, Switzerland) · 2014Article
- Article
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Authors and funding
6 authors at 4 institutions in 1 country.
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Abstract
Camalexin, the phytoalexin produced in the model plant Arabidopsis thaliana, possesses antiproliferative and cancer chemopreventive effects. We have demonstrated that the cytostatic/cytotoxic effects of camalexin on several prostate cancer (PCa) cells are due to oxidative stress. Lysosomes are vulnerable organelles to Reactive Oxygen Species (ROS)-induced injuries, with the potential to initiate and or facilitate apoptosis subsequent to release of proteases such as cathepsin D (CD) into the cytosol. We therefore hypothesized that camalexin reduces cell viability in PCa cells via alterations in expression and activity of CD. Cell viability was evaluated by MTS cell proliferation assay in LNCaP and ARCaP Epithelial (E) cells, and their respective aggressive sublines C4-2 and ARCaP Mesenchymal (M) cells, whereby the more aggressive PCa cells (C4-2 and ARCaPM) displayed greater sensitivity to camalexin treatments than the lesser aggressive cells (LNCaP and ARCaPE). Immunocytochemical analysis revealed CD relocalization from the lysosome to the cytosol subsequent to camalexin treatments, which was associated with increased protein expression of mature CD; p53, a transcriptional activator of CD; BAX, a downstream effector of CD, and cleaved PARP, a hallmark for apoptosis. Therefore, camalexin reduces cell viability via CD and may present as a novel therapeutic agent for treatment of metastatic prostate cancer cells.
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