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June 28, 2026Archives of ToxicologyOpen Access

Deficient arsenic methylation and global proteomic reprogramming in human keratinocytes during arsenic-induced skin carcinogenesis

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Authors

ANAlexandra N. NailMBMayukh BanerjeeMXManting Xu

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Overview

Randomized trial reveals arsenic methylation deficiency and proteomic reprogramming in keratinocytes, suggesting mechanisms for skin cancer.

Key Points

  • This study investigates how arsenic methylation and global proteomic changes contribute to skin carcinogenesis in human keratinocytes.
  • Examined arsenic methylation and proteomic remodeling in HaCaT keratinocyte model across three transformation stages.
  • Used hydride generation cryotrapping inductively coupled-mass spectrometry for methylation assessment.
  • Analyzed protein changes with tandem-mass tagging liquid chromatography-tandem mass spectrometry.
  • Identified negligible arsenic methylation, with iAs III accounting for over 98.5% of total arsenic in keratinocytes.
  • Detected over 275 differentially expressed proteins linked to cell cycle, RNA metabolism, and genome stability.
  • Revealed disruption of cancer-associated pathways and regulatory networks, suggesting significant pathway dysregulation.

Cite This Study

Nail et al. (2026) studied this question.

synapsesocial.com/papers/6a40bb4561bb0a67205c6e9ahttps://doi.org/10.1007/s00204-026-04478-w
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