ArticleOncogene2020
Pharmacologically targetable vulnerability in prostate cancer carrying RB1-SUCLA2 deletion.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The trial behind it
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- The Role of Long Noncoding RNAs in Modulation of Stress Granules in Cancer.Journal of cellular and molecular medicine · 2026Review
- Article
- Regulators of Cancer Progression: Succinylation.Cancers · 2025Review
- Decoding chromosomal instability insights in CRC by integrating omics and patient-derived organoids.Journal of experimental & clinical cancer research : CR · 2025Article
- Cholesterol synthesis is essential for the growth of liver metastasis-prone colorectal cancer cells.Cancer science · 2024Article
- Review
- Therapeutic Strategies for RB1-Deficient Cancers: Intersecting Gene Regulation and Targeted Therapy.Cancers · 2024Review
- SUCLG2 Regulates Mitochondrial Dysfunction through Succinylation in Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Transcriptomics and metabolomics study in mouse kidney of the molecular mechanism underlying energy metabolism response to hypoxic stress in highland areas.Experimental and therapeutic medicine · 2023Article
- Succinyl-CoA ligase ADP-forming subunit beta promotes stress granule assembly to regulate redox and drive cancer metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- TargetingCancers · 2021Review
- On the Origin of ATP Synthesis in Cancer.iScience · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RB1 gene is often homozygously deleted or mutated in prostate adenocarcinomas following acquirement of castration resistance and/or metastatic ability. We found that SUCLA2 gene is frequently involved in the deletion of the RB1 gene region in advanced prostate cancer. SUCLA2 constitutes the β-subunit of succinate CoA ligase heterodimer that reversibly converts succinyl CoA into succinate. We sought the possibility that deletion of SUCLA2 gives rise to a metabolic vulnerability that could be targeted therapeutically. We found a significant metabolic shift in SUCLA2-deleted prostate cancer cells, including lower mitochondrial respiratory activity. By screening a number of libraries for compounds that induce cell death selectively in SUCLA2-deficient prostate cancer cells, we identified thymoquinone (2-isopropyl-5-methylbenzo-1,4-quinone) and PMA (phorbol-12-myristate-13-acetate) from a natural compound library. These findings indicate that the metabolic vulnerability in SUCLA2-deficient prostate cancer cells is pharmacologically targetable.
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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.