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

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-re...

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Main Authors: Wang Jingyang, Yuan Zhixiang, Chen Taoyu, Guo Jiaqi, Qu Ying, Hou Tao, Zhu Lvyun, Shao Tong
Format: Article
Language:English
Published: EDP Sciences 2025-01-01
Series:E3S Web of Conferences
Online Access:https://www.e3s-conferences.org/articles/e3sconf/pdf/2025/37/e3sconf_emer2025_02013.pdf
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author Wang Jingyang
Yuan Zhixiang
Chen Taoyu
Guo Jiaqi
Qu Ying
Hou Tao
Zhu Lvyun
Shao Tong
author_facet Wang Jingyang
Yuan Zhixiang
Chen Taoyu
Guo Jiaqi
Qu Ying
Hou Tao
Zhu Lvyun
Shao Tong
author_sort Wang Jingyang
collection DOAJ
description 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.
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spelling doaj-art-1bad7b3fa75e4cfdbc1e9a9a47ea70ca2025-08-20T03:12:46ZengEDP SciencesE3S Web of Conferences2267-12422025-01-016370201310.1051/e3sconf/202563702013e3sconf_emer2025_02013Investigation of the impact of ultraviolet B irradiation on apoptosis and proliferation in A375 melanoma cellsWang Jingyang0Yuan Zhixiang1Chen Taoyu2Guo Jiaqi3Qu Ying4Hou Tao5Zhu Lvyun6Shao Tong7Department of Biology and Chemistry, College of Sciences, National University of Defense TechnologyDepartment of Biology and Chemistry, College of Sciences, National University of Defense TechnologyDepartment of Biology and Chemistry, College of Sciences, National University of Defense TechnologyDepartment of Biology and Chemistry, College of Sciences, National University of Defense TechnologyDepartment of Biology and Chemistry, College of Sciences, National University of Defense TechnologyDepartment of Oncology, The Second Xiangya Hospital, Central South UniversityDepartment of Biology and Chemistry, College of Sciences, National University of Defense TechnologyDepartment of Biology and Chemistry, College of Sciences, National University of Defense TechnologyThe 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.https://www.e3s-conferences.org/articles/e3sconf/pdf/2025/37/e3sconf_emer2025_02013.pdf
spellingShingle Wang Jingyang
Yuan Zhixiang
Chen Taoyu
Guo Jiaqi
Qu Ying
Hou Tao
Zhu Lvyun
Shao Tong
Investigation of the impact of ultraviolet B irradiation on apoptosis and proliferation in A375 melanoma cells
E3S Web of Conferences
title Investigation of the impact of ultraviolet B irradiation on apoptosis and proliferation in A375 melanoma cells
title_full Investigation of the impact of ultraviolet B irradiation on apoptosis and proliferation in A375 melanoma cells
title_fullStr Investigation of the impact of ultraviolet B irradiation on apoptosis and proliferation in A375 melanoma cells
title_full_unstemmed Investigation of the impact of ultraviolet B irradiation on apoptosis and proliferation in A375 melanoma cells
title_short Investigation of the impact of ultraviolet B irradiation on apoptosis and proliferation in A375 melanoma cells
title_sort investigation of the impact of ultraviolet b irradiation on apoptosis and proliferation in a375 melanoma cells
url https://www.e3s-conferences.org/articles/e3sconf/pdf/2025/37/e3sconf_emer2025_02013.pdf
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