Ning Ma , Yang Wang , Xin Li , Meiling Xu , Dandan Tan
{"title":"活性氧在癌症中的作用:机制见解和治疗创新。","authors":"Ning Ma , Yang Wang , Xin Li , Meiling Xu , Dandan Tan","doi":"10.1016/j.cstres.2025.100108","DOIUrl":null,"url":null,"abstract":"<div><div>Reactive oxygen species (ROS), once considered mere metabolic byproducts, are now recognized as crucial elements in the complex behavior of cancer, influencing both its progression and vulnerabilities. In healthy cells, ROS maintains a delicate balance: while small amounts are essential for signaling, excessive quantities can cause damage. Cancer disrupts this equilibrium, leveraging ROS to promote proliferation, metastasis, and survival, while employing antioxidant defenses to prevent self-destruction. It is the balance of ROS that is key to cancer growth: as they initiate cancer-related processes such as Mitogen-Activated Protein Kinase (MAPK), PI3K/Akt, and c-Jun N-terminal Kinase (JNK) pathways, and induce inflammation through NF-κB. Additionally, matrix metalloproteinases (MMPs) and vascular endothelial growth factor (VEGF) break down tissue barriers, fostering a tumor microenvironment (TME) conducive to cancer spread. However, this dependence on ROS presents a dual challenge. The timing, location, and quantity of radical formation, along with the surrounding cellular environment, determine whether ROS facilitate cancer progression or lead to cancer cell death. Disrupting this delicate balance of ROS may reveal new treatment methods, transforming cancer's survival mechanisms into significant weaknesses. This study explores the dual roles of ROS in cancer, examining how their contrasting effects impact tumor growth and revealing unexpected opportunities to shift the balance from growth to vulnerability.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":"30 5","pages":"Article 100108"},"PeriodicalIF":3.2000,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Reactive oxygen species in cancer: Mechanistic insights and therapeutic innovations\",\"authors\":\"Ning Ma , Yang Wang , Xin Li , Meiling Xu , Dandan Tan\",\"doi\":\"10.1016/j.cstres.2025.100108\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Reactive oxygen species (ROS), once considered mere metabolic byproducts, are now recognized as crucial elements in the complex behavior of cancer, influencing both its progression and vulnerabilities. In healthy cells, ROS maintains a delicate balance: while small amounts are essential for signaling, excessive quantities can cause damage. Cancer disrupts this equilibrium, leveraging ROS to promote proliferation, metastasis, and survival, while employing antioxidant defenses to prevent self-destruction. It is the balance of ROS that is key to cancer growth: as they initiate cancer-related processes such as Mitogen-Activated Protein Kinase (MAPK), PI3K/Akt, and c-Jun N-terminal Kinase (JNK) pathways, and induce inflammation through NF-κB. Additionally, matrix metalloproteinases (MMPs) and vascular endothelial growth factor (VEGF) break down tissue barriers, fostering a tumor microenvironment (TME) conducive to cancer spread. However, this dependence on ROS presents a dual challenge. The timing, location, and quantity of radical formation, along with the surrounding cellular environment, determine whether ROS facilitate cancer progression or lead to cancer cell death. Disrupting this delicate balance of ROS may reveal new treatment methods, transforming cancer's survival mechanisms into significant weaknesses. This study explores the dual roles of ROS in cancer, examining how their contrasting effects impact tumor growth and revealing unexpected opportunities to shift the balance from growth to vulnerability.</div></div>\",\"PeriodicalId\":9684,\"journal\":{\"name\":\"Cell Stress & Chaperones\",\"volume\":\"30 5\",\"pages\":\"Article 100108\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2025-08-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Stress & Chaperones\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1355814525000537\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Stress & Chaperones","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1355814525000537","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
Reactive oxygen species in cancer: Mechanistic insights and therapeutic innovations
Reactive oxygen species (ROS), once considered mere metabolic byproducts, are now recognized as crucial elements in the complex behavior of cancer, influencing both its progression and vulnerabilities. In healthy cells, ROS maintains a delicate balance: while small amounts are essential for signaling, excessive quantities can cause damage. Cancer disrupts this equilibrium, leveraging ROS to promote proliferation, metastasis, and survival, while employing antioxidant defenses to prevent self-destruction. It is the balance of ROS that is key to cancer growth: as they initiate cancer-related processes such as Mitogen-Activated Protein Kinase (MAPK), PI3K/Akt, and c-Jun N-terminal Kinase (JNK) pathways, and induce inflammation through NF-κB. Additionally, matrix metalloproteinases (MMPs) and vascular endothelial growth factor (VEGF) break down tissue barriers, fostering a tumor microenvironment (TME) conducive to cancer spread. However, this dependence on ROS presents a dual challenge. The timing, location, and quantity of radical formation, along with the surrounding cellular environment, determine whether ROS facilitate cancer progression or lead to cancer cell death. Disrupting this delicate balance of ROS may reveal new treatment methods, transforming cancer's survival mechanisms into significant weaknesses. This study explores the dual roles of ROS in cancer, examining how their contrasting effects impact tumor growth and revealing unexpected opportunities to shift the balance from growth to vulnerability.
期刊介绍:
Cell Stress and Chaperones is an integrative journal that bridges the gap between laboratory model systems and natural populations. The journal captures the eclectic spirit of the cellular stress response field in a single, concentrated source of current information. Major emphasis is placed on the effects of climate change on individual species in the natural environment and their capacity to adapt. This emphasis expands our focus on stress biology and medicine by linking climate change effects to research on cellular stress responses of animals, micro-organisms and plants.