UVA Irradiation Promotes Melanoma Cell Proliferation Mediated by OPN3 Independently of ROS Production.

IF 3.9 3区 医学 Q2 CELL BIOLOGY Pigment Cell & Melanoma Research Pub Date : 2024-10-30 DOI:10.1111/pcmr.13206
Yulei Zhang, Wen Zeng, Wei Zhang, Yu Wang, Shuqi Jin, Ting Liu, Huanhuan Luo, Hongguang Lu
{"title":"UVA Irradiation Promotes Melanoma Cell Proliferation Mediated by OPN3 Independently of ROS Production.","authors":"Yulei Zhang, Wen Zeng, Wei Zhang, Yu Wang, Shuqi Jin, Ting Liu, Huanhuan Luo, Hongguang Lu","doi":"10.1111/pcmr.13206","DOIUrl":null,"url":null,"abstract":"<p><p>UVA radiation, a primary risk factor in melanoma progression, partly acts through the mediation of reactive oxygen species (ROS). The role of ROS in driving cutaneous melanoma toward an invasive phenotype and whether it occurs through opsins (OPNs), which are photosensitive G protein-coupled receptors, is not fully understood. This study focuses on the impact of UVA radiation on melanoma cell proliferation, with a special emphasis on OPN3. Investigating the biphasic response to various UVA doses (0.75-9 J/cm<sup>2</sup>) in A375 and MV3 cell lines, and using EdU and CCK-8 assays, we observed dose-dependent changes in cell proliferation. Interestingly, UVA irradiation at these doses of 0.75, 1.5 and 3 J/cm<sup>2</sup> did not significantly induce ROS production. Our study further delves into the role of OPN3, a photosensitive receptor, in melanoma progression. Following UVA exposure, an increase in OPN3 expression was observed in melanoma cells lines A375 and MV3, indicating its role as a UVA-sensitive sensor and its influence on cell proliferation. Additionally, UVA-induced calcium flux in two melanoma cells lines pointed to a calcium-dependent G protein-coupled pathway in melanoma proliferation, mediated by OPN3 and not reliant on ROS. This research sheds light on the mechanism of UVA-induced melanoma progression, underscoring OPN3 as a pivotal regulator and advancing our understanding of UVA's interaction with opsins in melanoma progression.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":" ","pages":""},"PeriodicalIF":3.9000,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pigment Cell & Melanoma Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/pcmr.13206","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

UVA radiation, a primary risk factor in melanoma progression, partly acts through the mediation of reactive oxygen species (ROS). The role of ROS in driving cutaneous melanoma toward an invasive phenotype and whether it occurs through opsins (OPNs), which are photosensitive G protein-coupled receptors, is not fully understood. This study focuses on the impact of UVA radiation on melanoma cell proliferation, with a special emphasis on OPN3. Investigating the biphasic response to various UVA doses (0.75-9 J/cm2) in A375 and MV3 cell lines, and using EdU and CCK-8 assays, we observed dose-dependent changes in cell proliferation. Interestingly, UVA irradiation at these doses of 0.75, 1.5 and 3 J/cm2 did not significantly induce ROS production. Our study further delves into the role of OPN3, a photosensitive receptor, in melanoma progression. Following UVA exposure, an increase in OPN3 expression was observed in melanoma cells lines A375 and MV3, indicating its role as a UVA-sensitive sensor and its influence on cell proliferation. Additionally, UVA-induced calcium flux in two melanoma cells lines pointed to a calcium-dependent G protein-coupled pathway in melanoma proliferation, mediated by OPN3 and not reliant on ROS. This research sheds light on the mechanism of UVA-induced melanoma progression, underscoring OPN3 as a pivotal regulator and advancing our understanding of UVA's interaction with opsins in melanoma progression.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
紫外线照射促进黑色素瘤细胞增殖与 ROS 生成无关,由 OPN3 介导。
UVA 辐射是导致黑色素瘤恶化的主要风险因素,其部分作用是通过活性氧(ROS)来实现的。目前还不完全清楚 ROS 在促使皮肤黑色素瘤形成侵袭性表型方面所起的作用,以及这种作用是否是通过对光敏感的 G 蛋白偶联受体 opsins(OPNs)产生的。本研究重点关注 UVA 辐射对黑色素瘤细胞增殖的影响,并特别强调 OPN3。通过研究 A375 和 MV3 细胞系对不同 UVA 剂量(0.75-9 J/cm2)的双相反应,并使用 EdU 和 CCK-8 检测法,我们观察到细胞增殖的变化与剂量有关。有趣的是,0.75、1.5 和 3 J/cm2 剂量的 UVA 照射并没有显著诱导 ROS 的产生。我们的研究进一步探讨了光敏受体 OPN3 在黑色素瘤进展中的作用。暴露于 UVA 后,在黑色素瘤细胞系 A375 和 MV3 中观察到 OPN3 的表达增加,这表明它作为 UVA 敏感传感器的作用及其对细胞增殖的影响。此外,两种黑色素瘤细胞系中 UVA 诱导的钙通量表明,黑色素瘤增殖过程中的钙依赖性 G 蛋白偶联通路由 OPN3 介导,而不依赖于 ROS。这项研究揭示了 UVA 诱导黑色素瘤发展的机制,强调了 OPN3 是一个关键的调节因子,并加深了我们对 UVA 与黑色素瘤发展过程中的蛋白相互作用的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Pigment Cell & Melanoma Research
Pigment Cell & Melanoma Research 医学-皮肤病学
CiteScore
8.90
自引率
2.30%
发文量
54
审稿时长
6-12 weeks
期刊介绍: Pigment Cell & Melanoma Researchpublishes manuscripts on all aspects of pigment cells including development, cell and molecular biology, genetics, diseases of pigment cells including melanoma. Papers that provide insights into the causes and progression of melanoma including the process of metastasis and invasion, proliferation, senescence, apoptosis or gene regulation are especially welcome, as are papers that use the melanocyte system to answer questions of general biological relevance. Papers that are purely descriptive or make only minor advances to our knowledge of pigment cells or melanoma in particular are not suitable for this journal. Keywords Pigment Cell & Melanoma Research, cell biology, melatonin, biochemistry, chemistry, comparative biology, dermatology, developmental biology, genetics, hormones, intracellular signalling, melanoma, molecular biology, ocular and extracutaneous melanin, pharmacology, photobiology, physics, pigmentary disorders
期刊最新文献
The Lipid Droplet Protein DHRS3 Is a Regulator of Melanoma Cell State. UVA Irradiation Promotes Melanoma Cell Proliferation Mediated by OPN3 Independently of ROS Production. Issue Information Bay 11-7082, an NF-κB Inhibitor, Prevents Post-Inflammatory Hyperpigmentation Through Inhibition of Inflammation and Melanogenesis. Low-Dose Baricitinib Plus Narrow-Band Ultraviolet B for the Treatment of Progressive Non-Segmental Vitiligo: A Prospective, Controlled, Open-Label Study.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1