Chronic arsenic exposure and hsa-miR-186 overexpression causes transcriptome-wide differential alternative splicing contributing to skin carcinogenesis in human HaCaT cell line.

ABSTRACT: Environmental arsenic exposure causes skin cancer. Overexpression of hsa-miR-186 (mir-186) accelerated the malignant transformation of human keratinocytes by inorganic arsenic (iAs). Dysregulated alternative splicing is a key driver of carcinogenesis. iAs exposure disrupts alternative splicing. miR-186 is predicted to target several broad-spectrum splice regulators. The impact of miR-186 overexpression on differential alternative splicing alone and together in combination with iAs exposure and how that contributes to skin carcinogenesis has never been studied. We address this knowledge gap by investigating the transcriptome-wide differential alternative splicing events in preclinical HaCaT human keratinocyte clonal lines overexpressing miR-186 or scrambled control vectors concomitantly exp

SUBMITTER: Banerjee M 

PROVIDER: S-EPMC12687470 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature