CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors
Abstract MYC oncogene overexpression/amplification is common in multiple human cancers, in which it regulates proliferation, apoptosis and cell metabolism, among other processes, and its expression associates with poor prognosis. Targeting MYC presents an exciting therapeutic possibility, but develo...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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Springer Nature
2018-05-01
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| Series: | EMBO Molecular Medicine |
| Online Access: | https://doi.org/10.15252/emmm.201809213 |
| _version_ | 1827015171783000064 |
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| author | Fernando Salvador Roger R Gomis |
| author_facet | Fernando Salvador Roger R Gomis |
| author_sort | Fernando Salvador |
| collection | DOAJ |
| description | Abstract MYC oncogene overexpression/amplification is common in multiple human cancers, in which it regulates proliferation, apoptosis and cell metabolism, among other processes, and its expression associates with poor prognosis. Targeting MYC presents an exciting therapeutic possibility, but developing appropriate drugs that impair protein function remains challenging. Searching for alternative therapeutic options for treating aggressive MYC‐driven cancers is thus of high clinical interest. Intriguingly, MYC‐driven cancers present vulnerability against spliceosome inhibition. In this issue of EMBO Molecular Medicine, Iwai et al (2018) tackle targeting the splicing regulatory Cdc2‐like kinase (CLKs) family. They report that a novel, orally administered CLK2 inhibitor (T‐025) induces exon skipping, which results in cancer cell growth reduction, especially in breast cancer (BCa) MYC‐driven tumors. |
| first_indexed | 2024-03-07T17:14:17Z |
| format | Article |
| id | doaj.art-d225e21f591c4e1ab04fc29ede715eb6 |
| institution | Directory Open Access Journal |
| issn | 1757-4676 1757-4684 |
| language | English |
| last_indexed | 2025-02-18T14:19:13Z |
| publishDate | 2018-05-01 |
| publisher | Springer Nature |
| record_format | Article |
| series | EMBO Molecular Medicine |
| spelling | doaj.art-d225e21f591c4e1ab04fc29ede715eb62024-10-28T08:56:06ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842018-05-011061310.15252/emmm.201809213CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumorsFernando Salvador0Roger R Gomis1Oncology Program, Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and TechnologyOncology Program, Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and TechnologyAbstract MYC oncogene overexpression/amplification is common in multiple human cancers, in which it regulates proliferation, apoptosis and cell metabolism, among other processes, and its expression associates with poor prognosis. Targeting MYC presents an exciting therapeutic possibility, but developing appropriate drugs that impair protein function remains challenging. Searching for alternative therapeutic options for treating aggressive MYC‐driven cancers is thus of high clinical interest. Intriguingly, MYC‐driven cancers present vulnerability against spliceosome inhibition. In this issue of EMBO Molecular Medicine, Iwai et al (2018) tackle targeting the splicing regulatory Cdc2‐like kinase (CLKs) family. They report that a novel, orally administered CLK2 inhibitor (T‐025) induces exon skipping, which results in cancer cell growth reduction, especially in breast cancer (BCa) MYC‐driven tumors.https://doi.org/10.15252/emmm.201809213 |
| spellingShingle | Fernando Salvador Roger R Gomis CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors EMBO Molecular Medicine |
| title | CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors |
| title_full | CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors |
| title_fullStr | CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors |
| title_full_unstemmed | CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors |
| title_short | CLK2 blockade modulates alternative splicing compromising MYC‐driven breast tumors |
| title_sort | clk2 blockade modulates alternative splicing compromising myc driven breast tumors |
| url | https://doi.org/10.15252/emmm.201809213 |
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