SMYD3 Impedes Small Cell Lung Cancer Sensitivity to Alkylation Damage through RNF113A Methylation-Phosphorylation Cross-talk.
Valentina LukinovićSimone HausmannGaël S RothClement OyeniranTanveer AhmadNing TsaoJoshua R BricknerAlexandre G CasanovaFlorent ChuffartAna Morales BenitezJessica VayrRebecca RodellMarianne TardifPascal W T C JansenYohann CoutMichiel VermeulenPierre HainautPawel K MazurNima MosammaparastNicolas ReynoirdPublished in: Cancer discovery (2022)
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.
Keyphrases
- induced apoptosis
- small cell lung cancer
- oxidative stress
- locally advanced
- signaling pathway
- genome wide
- dna methylation
- endoplasmic reticulum stress
- cell cycle arrest
- machine learning
- electronic health record
- dna damage response
- poor prognosis
- cell proliferation
- deep learning
- big data
- rectal cancer
- brain metastases
- radiation therapy
- cell death
- data analysis
- neural network