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

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

  • By

  • Alexandra N. Nail

  • Mayukh Banerjee

  • Manting Xu

  • Caitlin H. Reynolds

  • Miroslav Stýblo

  • Peter H. Cable

  • Daniel W. Wilkey

  • Michael L. Merchant

  • Ana P. Ferragut Cardoso

  • Shelia D. Thomas

  • J. Christopher States

  • June 27, 2026

  • 0 min

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  • 1

    Chronic exposure to inorganic arsenic affects approximately 220 million people and is linked to non-melanoma skin cancer development.

  • 2

    HaCaT cells exposed to inorganic arsenite for 28 weeks transform into an aggressive cSCC-like phenotype and can form tumors in immunocompromised mice.

  • 3

    Comprehensive longitudinal proteomic profiling is necessary to understand the protein expression changes during iAsIII-induced malignant transformation.

  • 4

    Arsenic methylation status may influence the molecular mechanisms driving keratinocyte malignant transformation, as HaCaT cells do not methylate iAsIII.

  • 5

    The study aims to assess arsenic metabolism across various human keratinocyte lines to identify key metabolites and molecular targets in arsenic-induced cSCC.

Original Source(s)

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

  • by Alexandra N. Nail, Mayukh Banerjee, Manting Xu, Caitlin H. Reynolds, Miroslav Stýblo, Peter H. Cable, Daniel W. Wilkey, Michael L. Merchant, Ana P. Ferragut Cardoso, Shelia D. Thomas, J. Christopher States

  • June 27, 2026

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