Molecular mechanisms behind ROS regulation in cancer: A balancing act between augmented tumorigenesis and cell apoptosis

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dc.contributor.authorTuli, Hardeep Singh
dc.contributor.authorKaur, Jagjit
dc.contributor.authorVashishth, Kanupriya
dc.contributor.authorSak, Katrin
dc.contributor.authorSharma, Ujjawal
dc.contributor.authorChoudhary, Renuka
dc.contributor.authorBehl, Tapan
dc.contributor.authorSingh, Tejveer
dc.contributor.authorSharma, Sheetu
dc.contributor.authorSaini, Adesh K.
dc.contributor.authorDhama, Kuldeep
dc.contributor.authorVarol, Mehmet
dc.contributor.authorSethi, Gautam
dc.date.accessioned2024-01-21T10:54:10Z
dc.date.accessioned2024-08-14T07:40:54Z
dc.date.available2024-01-21T10:54:10Z
dc.date.available2024-08-14T07:40:54Z
dc.date.issued2022-11-28T00:00:00
dc.description.abstractROS include hydroxyl radicals (HO.), superoxide (O2.), and hydrogen peroxide (H2O2). ROS are typically produced under physiological conditions and play crucial roles in living organisms. It is known that ROS, which are created spontaneously by cells through aerobic metabolism in mitochondria, can have either a beneficial or detrimental influence on biological systems. Moderate levels of ROS can cause oxidative damage to proteins, DNA and lipids, which can aid in the pathogenesis of many disorders, including cancer. However, excessive concentrations of ROS can initiate programmed cell death in cancer. Presently, a variety of chemotherapeutic drugs and herbal agents are being investigated to induce ROS-mediated cell death in cancer. Therefore, preserving ROS homeostasis is essential for ensuring normal cell development and survival. On account of a significant association of ROS levels at various concentrations with carcinogenesis in a number of malignancies, further studies are needed to determine the underlying molecular mechanisms and develop the possibilities for intervening in these processes. � 2022, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.en_US
dc.identifier.doi10.1007/s00204-022-03421-z
dc.identifier.issn3405761
dc.identifier.urihttp://10.2.3.109/handle/32116/4234
dc.identifier.urlhttps://link.springer.com/10.1007/s00204-022-03421-z
dc.language.isoen_USen_US
dc.publisherSpringer Science and Business Media Deutschland GmbHen_US
dc.subjectAngiogenesisen_US
dc.subjectApoptosisen_US
dc.subjectCanceren_US
dc.subjectInflammationen_US
dc.subjectMetastasisen_US
dc.subjectmiRNAen_US
dc.subjectROSen_US
dc.titleMolecular mechanisms behind ROS regulation in cancer: A balancing act between augmented tumorigenesis and cell apoptosisen_US
dc.title.journalArchives of Toxicologyen_US
dc.typeReviewen_US
dc.type.accesstypeClosed Accessen_US

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