SMYD3 Impedes Small Cell Lung Cancer Sensitivity to Alkylation Damage through RNF113A Methylation–Phosphorylation Cross-talk Article Swipe
Valentina Lukinović
,
Simone Hausmann
,
Gaël Roth
,
Clément Oyeniran
,
Tanveer Ahmad
,
Ning Tsao
,
Joshua R. Brickner
,
Alexandre G. Casanova
,
Florent Chuffart
,
Ana Morales Benitez
,
Jessica Vayr
,
Rebecca Rodell
,
Marianne Tardif
,
Pascal W.T.C. Jansen
,
Yohann Couté
,
Michiel Vermeulen
,
Pierre Hainaut
,
Paweł K. Mazur
,
Nima Mosammaparast
,
Nicolas Reynoird
·
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1158/2159-8290.cd-21-0205
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1158/2159-8290.cd-21-0205
Small cell lung cancer (SCLC) is the most fatal form of lung cancer, with dismal survival, limited therapeutic options, and rapid development of chemoresistance. We identified the lysine methyltransferase SMYD3 as a major regulator of SCLC sensitivity to alkylation-based chemotherapy. RNF113A methylation by SMYD3 impairs its interaction with the phosphatase PP4, controlling its phosphorylation levels. This cross-talk between posttranslational modifications acts as a key switch in promoting and maintaining RNF113A E3 ligase activity, essential for its role in alkylation damage response. In turn, SMYD3 inhibition restores SCLC vulnerability to alkylating chemotherapy. Our study sheds light on a novel role of SMYD3 in cancer, uncovering this enzyme as a mediator of alkylation damage sensitivity and providing a rationale for small-molecule SMYD3 inhibition to improve responses to established chemotherapy. Significance: SCLC rapidly becomes resistant to conventional chemotherapy, leaving patients with no alternative treatment options. Our data demonstrate that SMYD3 upregulation and RNF113A methylation in SCLC are key mechanisms that control the alkylation damage response. Notably, SMYD3 inhibition sensitizes cells to alkylating agents and promotes sustained SCLC response to chemotherapy. This article is highlighted in the In This Issue feature, p. 2007
Related Topics
Concepts
Cancer research
Methylation
Methyltransferase
Biology
Lung cancer
Ubiquitin ligase
Ubiquitin
Medicine
Oncology
Biochemistry
Gene
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1158/2159-8290.cd-21-0205
- https://aacrjournals.org/cancerdiscovery/article-pdf/12/9/2158/3203638/2158.pdf
- OA Status
- hybrid
- Cited By
- 27
- References
- 58
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4285042270
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4285042270Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1158/2159-8290.cd-21-0205Digital Object Identifier
- Title
-
SMYD3 Impedes Small Cell Lung Cancer Sensitivity to Alkylation Damage through RNF113A Methylation–Phosphorylation Cross-talkWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2022Year of publication
- Publication date
-
2022-07-12Full publication date if available
- Authors
-
Valentina Lukinović, Simone Hausmann, Gaël Roth, Clément Oyeniran, Tanveer Ahmad, Ning Tsao, Joshua R. Brickner, Alexandre G. Casanova, Florent Chuffart, Ana Morales Benitez, Jessica Vayr, Rebecca Rodell, Marianne Tardif, Pascal W.T.C. Jansen, Yohann Couté, Michiel Vermeulen, Pierre Hainaut, Paweł K. Mazur, Nima Mosammaparast, Nicolas ReynoirdList of authors in order
- Landing page
-
https://doi.org/10.1158/2159-8290.cd-21-0205Publisher landing page
- PDF URL
-
https://aacrjournals.org/cancerdiscovery/article-pdf/12/9/2158/3203638/2158.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
hybridOpen access status per OpenAlex
- OA URL
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https://aacrjournals.org/cancerdiscovery/article-pdf/12/9/2158/3203638/2158.pdfDirect OA link when available
- Concepts
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Cancer research, Methylation, Methyltransferase, Biology, Lung cancer, Ubiquitin ligase, Ubiquitin, Medicine, Oncology, Biochemistry, GeneTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
27Total citation count in OpenAlex
- Citations by year (recent)
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2025: 3, 2024: 18, 2023: 6Per-year citation counts (last 5 years)
- References (count)
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58Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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