ArticleClinical epigenetics2026
Epigenome-wide association study of leukocyte telomere length and their effects on smoking-induced lung tumorigenesis: insights from the Dongfeng-Tongji cohort study.
Article in Clinical epigenetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundEpigenetic factors underlying telomere length (TL) may provide insight into telomeric homeostasis, with direct links to cigarette smoking and lung cancer susceptibility. It is unclear, nevertheless, to what extent effects of TL and its related DNA methylation on the smoking-induced lung tumorigenesis.
methodsA case-cohort study is performed within the Dongfeng-Tongji (DFTJ) cohort, including a randomly selected subcohort of 1399 subjects and 359 incident lung cancer cases. We use a linear regression model to conduct EWAS of TL, while the associations of TL and candidate CpGs with lung cancer risk are evaluated using weighted Cox proportional hazard regression models. Furthermore, the causal inference test (CIT) and mediation analysis are used to elucidate the causality of TL and its relevant CpGs in the smoking-induced lung tumorigenesis. The methylation-expression associations are assessed in SY panel (n = 144), adjacent normal lung tissues (n = 32) and solid normal tissues in TCGA (n = 375).
resultsWe identified 31 CpGs with significant associations with TL at FDR < 0.05, and their annotated genes are mainly enriched in oxidative stress, energy metabolism and immunity regulation pathways. Among the 31 TL-related CpGs, 3 CpGs showed substantial associations with both lung cancer risk and smoking status (all FDR < 0.1), including cg26563141 in RGPD1/RGPD2, cg03964851in MIR1974/KIAA0825, and cg08976633 in ZNF74. The further mediation analyses suggest that these three CpGs could mediate 2.89%~8.83% effect on lung cancer risk induced by smoking (all FDR < 0.1). The further CIT and multiple mediation analysis reveal that the effect of smoking on lung cancer risk is primarily mediated by TL (> 10%) while being mildly mediated via DNA methylation pathway (< 1%). Also, hypermethylation of cg26563141 is related to low expression of RGPD1 and RGPD2 across blood and tissue samples.
conclusionsBoth TL attrition and the three candidate CpGs showed significant mediation effects on lung cancer risk induced by smoking. These findings provide novel insight into the epigenetic control of telomere homeostasis mechanisms and clues for methylation alteration and TL in smoking-induced lung tumorigenesis.
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