Investigation of the impact of ultraviolet B irradiation on apoptosis and proliferation in A375 melanoma cells

¹ Department of Biology and Chemistry, College of Sciences, National University of Defense Technology, Changsha, 410073, China
² Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, 410012, China

^* Corresponding author: Tao Shao, E-mail: shaotong@zju.edu.cn;
^* Lvyun Zhu, E-mail: zhulvyun@nudt.edu.cn

Abstract

The increasing environmental impact of ultraviolet B (UVB) radiation, exacerbated by ozone layer depletion and anthropogenic influences, highlights its dual threat to ecological balance and human health. This study examines the cytotoxic mechanisms induced by UVB in A375 melanoma cells using dose-response assays and multi-omics analysis. UVB exposure resulted in dose-dependent apoptosis and proliferation arrest, with irreversible cell cycle collapse observed at 48 hours. Transcriptomic analysis identified 303 differentially expressed genes, with p53 signaling emerging as the central regulator. UVB- activated p53 induced G2/M arrest through p21-mediated inhibition of CDK1/cyclin B, while simultaneous suppression of PI3K-AKT signaling and pyrimidine metabolism disrupted survival pathways and DNA repair, creating a self-reinforcing cytotoxic cascade. Notably, two previously uncharacterized genes were significantly downregulated, suggesting their potential roles in UVB stress adaptation. Functional validation confirmed the dysregulation of mitosis and adhesion pathways. These findings not only advance mechanistic insights into melanoma pathobiology but also propose actionable therapeutic strategies. Furthermore, the conserved stress responses identified here may inform ecological risk assessments, as UVB-driven molecular disruptions in melanoma cells mirror vulnerabilities observed in environmentally sensitive species like phytoplankton.