ArticleCancer research2011
Carminomycin I is an apoptosis inducer that targets the Golgi complex in clear cell renal carcinoma cells.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Highly accurate protein structure prediction-based virtual docking pipeline accelerating the identification of anti-schistosomal compounds.PLoS pathogens · 2025Article
- SMGL-1/NBAS acts as a RAB-8 GEF to regulate unconventional protein secretion.The Journal of cell biology · 2022Article
- Golgi Structure and Function in Health, Stress, and Diseases.Results and problems in cell differentiation · 2019Review
- Next Generation Sequencing in Renal Cell Carcinoma: Towards Precision Medicine.Kidney cancer journal : official journal of the Kidney Cancer Association · 2019Article
- Englerin A Inhibits EWS-FLI1 DNA Binding in Ewing Sarcoma Cells.The Journal of biological chemistry · 2016Article
- Natural compounds regulate glycolysis in hypoxic tumor microenvironment.BioMed research international · 2015Review
- Renal cancer-selective Englerin A induces multiple mechanisms of cell death and autophagy.Journal of experimental & clinical cancer research : CR · 2013Article
- Cripto-1 enhances the canonical Wnt/β-catenin signaling pathway by binding to LRP5 and LRP6 co-receptors.Cellular signalling · 2013Article
- Lack of a functional VHL gene product sensitizes renal cell carcinoma cells to the apoptotic effects of the protein synthesis inhibitor verrucarin A.Neoplasia (New York, N.Y.) · 2012Article
- Analysis of apoptosis methods recently used in Cancer Research and Cell Death & Disease publications.Cell death & disease · 2012Article
- Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Clear cell renal cell carcinoma (CCRCC) evolves due to mutations in the Von Hippel-Lindau (VHL) tumor suppressor gene. Although the loss of VHL enables survival and proliferation of CCRCC cells, it is also expected to introduce vulnerabilities that may be exploited for therapeutics discovery. To this end, we developed a high-throughput screen to identify small molecules derived from plants, microorganisms, and marine organisms to which CCRCC cells are sensitive. Screening over 8,000 compounds using this approach, we report here the identification of the microbially derived compound carminomycin I (CA) as an effective inhibitor of VHL-defective (VHL(-/-)) CCRCC cell proliferation. CA also induced apoptosis in CCRCC cells by a mechanism independent of p53 or hypoxia-inducible factor 2. We found that P-glycoprotein (P-gp) sequestered CA within the Golgi complex. Interestingly, Golgi sequestration was critical for the antiproliferative effects of CA and P-gp inhibitors abrogated this activity. Furthermore, CA induced cleavage of the Golgi protein p115 and the translocation of its C-terminal fragment to the nucleus. Finally, examination of the activity of the VHL-interacting Golgi protein, endoplasmic reticulum-Golgi intermediate compartment, ERGIC-53 showed that VHL could mediate protection from CA in CCRCC cells. Our natural product-based screening approach has revealed the P-gp-mediated localization of anticancer compounds within the Golgi in CCRCC cells as a potential strategy of targeting VHL-deficient CCRCC cells.
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Registered trials
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