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In 2003, ADAR1 (Adenosine Deaminase 1 Acting on dsRNA) was identified as the disease gene for an autosomal dominant disease — dyschromatosis symmetrica hereditaria (DSH) — which is characterized by a mixture of hyperpigmented and hypopigmented macules that are distributed on the dorsal aspects of the extremities and freckle-like macules on the face. To date, more than 100 ADAR1 mutations have been discovered in DSH patients. However, the exact molecular pathogenesis of DSH has not been clearly identified. To investigate the effects of ADAR1 mutations on the signal transduction pathway of melanogenesis, we used the RNA interference (RNAi) method to knockdown ADAR1 in human keratinocyte HaCaT cells, and determined a hormone precursor peptide proopiomelanocortin (POMC) expression in the ADAR1-knockdown HaCaT cells. Based on the results, we found that ADAR1 knockdown inhibits POMC expression in HaCaT cells. The findings of the present study imply that ADAR1 plays an important role in regulating POMC expression in keratinocytes, and possibly, the UV-induced pigmentation of skin.

Knockdown of Adenosine Deaminase 1 Acting on dsRNA Inhibits Expression of Proopiomelanocortin in HaCaT Cells