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Article

KRAS-mediated CCDC6 degradation drives xCT upregulation and ferroptosis evasion.

Apoptosis : an international journal on programmed cell death - 14 Jul 2026

Criscuolo Daniela, Catalano Rosaria, Baviello Carmela, Fioravanti Claudia, Vigliar Elena, Morra Francesco, Marotta Maria, Mimura Junsei, Iaccarino Antonino, Pepe Francesco, Belotti Dorina, Troncone Giancarlo, Merolla Francesco, Melillo Rosa Marina, Celetti Angela

Abstract excerpt

Oncogenic KRAS mutations drive tumorigenesis by promoting pro-survival signaling and metabolic reprogramming, including the maintenance of redox balance to evade oxidative stress. A key mechanism involves the upregulation of the xCT cystine/glutamate antiporter, which sustains glutathione (GSH) synthesis and protects cells from oxidative damage and ferroptosis. While it is known that the ETS1-ATF4 complex...

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Share to Activating Transcription Factor 4
Share to Ferroptosis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Glycogen Synthase Kinase 3 beta

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Source

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Identifiers

PMID: 42448954
DOI: 10.1007/s10495-026-02400-4
PMCID: PMC13369686

Genes

KRAS
CCDC6
ATF4
ETS1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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KRAS-mediated CCDC6 degradation drives xCT upregulation and ferroptosis evasion.PMID 42448954Read ↗

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