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Page 1
Arginine reprograms metabolism in liver cancer via RBM39.
Mossmann D, Müller C, Park S, Ryback B, Colombi M, Ritter N, Weißenberger D, Dazert E, Coto-Llerena M, Nuciforo S, Blukacz L, Ercan C, Jimenez V, Piscuoglio S, Bosch F, Terracciano LM, Sauer U, Heim MH, Hall MN. Mossmann D, et al. Cell. 2023 Nov 9;186(23):5068-5083.e23. doi: 10.1016/j.cell.2023.09.011. Epub 2023 Oct 6. Cell. 2023. PMID: 37804830 Free PMC article.
Metabolic reprogramming is a hallmark of cancer. However, mechanisms underlying metabolic reprogramming and how altered metabolism in turn enhances tumorigenicity are poorly understood. ...Mechanistically, arginine binds RNA-binding motif protein 39 (RBM39) to contr …
Metabolic reprogramming is a hallmark of cancer. However, mechanisms underlying metabolic reprogramming and how altered metabolism in …
RNA-binding motif protein 39 (RBM39): An emerging cancer target.
Xu Y, Nijhuis A, Keun HC. Xu Y, et al. Br J Pharmacol. 2022 Jun;179(12):2795-2812. doi: 10.1111/bph.15331. Epub 2021 Jan 3. Br J Pharmacol. 2022. PMID: 33238031 Free article. Review.
Recent studies have revealed that RBM39 is the unexpected target of aryl sulphonamides, which act as molecular glues between RBM39 and the DCAF15-associated E3 ubiquitin ligase complex leading to selective degradation of the target. ...Many clinical studies have sho …
Recent studies have revealed that RBM39 is the unexpected target of aryl sulphonamides, which act as molecular glues between RBM39 …
Systematic pan-cancer analysis identifies RBM39 as an immunological and prognostic biomarker.
Zhang R, Wang W, Zhang N, Chen X, Liu W, Zhang L, Liu N. Zhang R, et al. J Cell Mol Med. 2022 Sep;26(18):4859-4871. doi: 10.1111/jcmm.17517. Epub 2022 Aug 21. J Cell Mol Med. 2022. PMID: 35989423 Free PMC article.
Our results showed that RBM39 is overexpressed in most cancers. RBM39 was positively or negatively correlated with the prognosis of different tumours. RBM39 expression was associated with TMB and MSI in 9 and 12 cancer types. ...
Our results showed that RBM39 is overexpressed in most cancers. RBM39 was positively or negatively correlated with the …
Anticancer sulfonamides target splicing by inducing RBM39 degradation via recruitment to DCAF15.
Han T, Goralski M, Gaskill N, Capota E, Kim J, Ting TC, Xie Y, Williams NS, Nijhawan D. Han T, et al. Science. 2017 Apr 28;356(6336):eaal3755. doi: 10.1126/science.aal3755. Epub 2017 Mar 16. Science. 2017. PMID: 28302793
Mutations in RBM39 that prevent its recruitment to CUL4-DCAF15 increase RBM39 stability and confer resistance to indisulam's cytotoxicity. RBM39 associates with precursor messenger RNA (pre-mRNA) splicing factors, and inactivation of RBM39 by indisulam …
Mutations in RBM39 that prevent its recruitment to CUL4-DCAF15 increase RBM39 stability and confer resistance to indisulam's c …
Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells.
Chen WC, To MD, Westcott PMK, Delrosario R, Kim IJ, Philips M, Tran Q, Bollam SR, Goodarzi H, Bayani N, Mirzoeva O, Balmain A. Chen WC, et al. Nat Commun. 2021 Jul 13;12(1):4288. doi: 10.1038/s41467-021-24498-7. Nat Commun. 2021. PMID: 34257283 Free PMC article.
KRAS4A splicing is controlled by the DCAF15/RBM39 pathway, and deletion of KRAS4A or pharmacological inhibition of RBM39 using Indisulam leads to inhibition of cancer stem cells. Our data identify existing clinical drugs that target KRAS4A splicing, and sugge …
KRAS4A splicing is controlled by the DCAF15/RBM39 pathway, and deletion of KRAS4A or pharmacological inhibition of RBM39 using …
Molecular basis of RNA-binding and autoregulation by the cancer-associated splicing factor RBM39.
Campagne S, Jutzi D, Malard F, Matoga M, Romane K, Feldmuller M, Colombo M, Ruepp MD, Allain FH. Campagne S, et al. Nat Commun. 2023 Sep 4;14(1):5366. doi: 10.1038/s41467-023-40254-5. Nat Commun. 2023. PMID: 37666821 Free PMC article.
Pharmacologic depletion of RNA-binding motif 39 (RBM39) using aryl sulfonamides represents a promising anti-cancer therapy but requires high levels of the adaptor protein DCAF15. ...Our results support a model where RRM2 selects the 3'-splice site of a poison exon a …
Pharmacologic depletion of RNA-binding motif 39 (RBM39) using aryl sulfonamides represents a promising anti-cancer therapy but …
The cancer-testis lncRNA LINC01977 promotes HCC progression by interacting with RBM39 to prevent Notch2 ubiquitination.
Xia A, Yue Q, Zhu M, Xu J, Liu S, Wu Y, Wang Z, Xu Z, An H, Wang Q, Wang S, Sun B. Xia A, et al. Cell Death Discov. 2023 May 18;9(1):169. doi: 10.1038/s41420-023-01459-1. Cell Death Discov. 2023. PMID: 37198207 Free PMC article.
Cancer-testis genes are involved in the occurrence and development of cancer, but the role of cancer-testis-associated lncRNAs (CT-lncRNAs) in hepatocellular carcinoma (HCC) remains to be explored. Here, we discovered a novel CT-lncRNA, LINC01977, based on th …
Cancer-testis genes are involved in the occurrence and development of cancer, but the role of cancer-testis-associated …
Pharmacologic modulation of RNA splicing enhances anti-tumor immunity.
Lu SX, De Neef E, Thomas JD, Sabio E, Rousseau B, Gigoux M, Knorr DA, Greenbaum B, Elhanati Y, Hogg SJ, Chow A, Ghosh A, Xie A, Zamarin D, Cui D, Erickson C, Singer M, Cho H, Wang E, Lu B, Durham BH, Shah H, Chowell D, Gabel AM, Shen Y, Liu J, Jin J, Rhodes MC, Taylor RE, Molina H, Wolchok JD, Merghoub T, Diaz LA Jr, Abdel-Wahab O, Bradley RK. Lu SX, et al. Cell. 2021 Jul 22;184(15):4032-4047.e31. doi: 10.1016/j.cell.2021.05.038. Epub 2021 Jun 24. Cell. 2021. PMID: 34171309 Free PMC article.
Although mutations in DNA are the best-studied source of neoantigens that determine response to immune checkpoint blockade, alterations in RNA splicing within cancer cells could similarly result in neoepitope production. However, the endogenous antigenicity and clinical po …
Although mutations in DNA are the best-studied source of neoantigens that determine response to immune checkpoint blockade, alterations in R …
E7820, an anti-cancer sulfonamide, degrades RBM39 in patients with splicing factor mutant myeloid malignancies: a phase II clinical trial.
Bewersdorf JP, Stahl M, Taylor J, Mi X, Chandhok NS, Watts J, Derkach A, Wysocki M, Lu SX, Bourcier J, Hogg SJ, Rahman J, Chaudhry S, Totiger TM, Abdel-Wahab O, Stein EM. Bewersdorf JP, et al. Leukemia. 2023 Dec;37(12):2512-2516. doi: 10.1038/s41375-023-02050-4. Epub 2023 Oct 9. Leukemia. 2023. PMID: 37814121 Free PMC article. Clinical Trial. No abstract available.
The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress.
Lemaitre F, Chakrama F, O'Grady T, Peulen O, Rademaker G, Deward A, Chabot B, Piette J, Colige A, Lambert C, Dequiedt F, Habraken Y. Lemaitre F, et al. Nucleic Acids Res. 2022 Dec 9;50(22):12768-12789. doi: 10.1093/nar/gkac1130. Nucleic Acids Res. 2022. PMID: 36477312 Free PMC article.
Genotoxic agents, that are used in cancer therapy, elicit the reprogramming of the transcriptome of cancer cells. ...Unexpectedly, inactivation of RBM39 in response to cisplatin involves its interaction with the AP-1 family transcription factor c-Jun that pre …
Genotoxic agents, that are used in cancer therapy, elicit the reprogramming of the transcriptome of cancer cells. ...Unexpecte …
53 results