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https://hdl.handle.net/2440/127198
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dc.contributor.author | Kohno, S. | - |
dc.contributor.author | Linn, P. | - |
dc.contributor.author | Nagatani, N. | - |
dc.contributor.author | Watanabe, Y. | - |
dc.contributor.author | Kumar, S. | - |
dc.contributor.author | Soga, T. | - |
dc.contributor.author | Takahashi, C. | - |
dc.date.issued | 2020 | - |
dc.identifier.citation | Oncogene, 2020; 39(34):5690-5707 | - |
dc.identifier.issn | 1476-5594 | - |
dc.identifier.issn | 1476-5594 | - |
dc.identifier.uri | http://hdl.handle.net/2440/127198 | - |
dc.description.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. | - |
dc.description.statementofresponsibility | Susumu Kohno, Paing Linn, Naoko Nagatani, Yoshihiro Watanabe, Sharad Kumar, Tomoyoshi Soga, Chiaki Takahashi | - |
dc.language.iso | en | - |
dc.publisher | Springer Nature | - |
dc.rights | © The Author(s), under exclusive licence to Springer Nature Limited 2020 | - |
dc.source.uri | http://dx.doi.org/10.1038/s41388-020-1381-6 | - |
dc.subject | Cell Line, Tumor | - |
dc.subject | Animals | - |
dc.subject | Mice, Knockout | - |
dc.subject | Humans | - |
dc.subject | Mice, Nude | - |
dc.subject | Mice, SCID | - |
dc.subject | Prostatic Neoplasms | - |
dc.subject | Tetradecanoylphorbol Acetate | - |
dc.subject | Benzoquinones | - |
dc.subject | Succinate-CoA Ligases | - |
dc.subject | Retinoblastoma Protein | - |
dc.subject | Apoptosis | - |
dc.subject | Gene Deletion | - |
dc.subject | Male | - |
dc.subject | HEK293 Cells | - |
dc.subject | PC-3 Cells | - |
dc.title | Pharmacologically targetable vulnerability in prostate cancer carrying RB1-SUCLA2 deletion | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1038/s41388-020-1381-6 | - |
dc.relation.grant | http://purl.org/au-research/grants/nhmrc/GNT1103006 | - |
pubs.publication-status | Published online | - |
dc.identifier.orcid | Kumar, S. [0000-0001-7126-9814] | - |
Appears in Collections: | Aurora harvest 8 Medicine publications |
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