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X-ray Irradiation Suppresses Keloid Growth by Inducing G2/M Arrest via the Phytosphingosine-KIF20A Axis

ABSTRACT: Keloid radiotherapy is clinically effective but has an incomplete underlying molecular mechanism and limited accessibility; we used X-ray exposure to identify effector pathways replicating its antifibrotic benefits without further radiation. After collecting patient keloid samples, primary human keloid fibroblasts and normal skin fibroblasts, non-targeted metabolomics and RNA-seq were performed, identifying phytosphingosine (PHS) and KIF20A as key mediators of fibrosis and cell death in keloid radiotherapy. X-ray irradiation increased PHS release in keloid fibroblasts; exogenous PHS and X-ray irradiation independently induced cell death and reduced fibrosis, their combination exerted radiosensitization by boosting G2/M arrest and apoptosis while lowering fibrosis progression, and both PHS and irradiation reduced KIF20A whose loss induced cell cycle arrest and apoptosis. Our findings reveal that X-ray irradiation enhances keloid fibroblast PHS secretion that downregulates KIF20A to exert keloid therapeutic effects, and topical PHS or KIF20A-targeting agents are immediately translatable alternatives for radiotherapy-ineligible patients.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS14461 | MetaboLights | 2026-06-06

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS14461_LC-MS_negative_reverse-phase.txt	Txt
	a_MTBLS14461_LC-MS_positive_reverse-phase.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS14461_LC-MS_negative_reverse-phase_v2_maf.tsv	Tabular
	m_MTBLS14461_LC-MS_positive_reverse-phase_v2_maf.tsv	Tabular

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