English

dc.contributor.authorGokbilen, SO
dc.contributor.authorBecer, E
dc.contributor.authorVatansever, HS
dc.date.accessioned2024-07-18T11:58:06Z
dc.date.available2024-07-18T11:58:06Z
dc.description.abstractPERGAMON-ELSEVIER SCIENCE LTD
dc.identifier.issn1879-0739
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/7269
dc.language.isoReview
dc.publisher0271-5317
dc.subjectCellular senescence plays a key role in aging and age-related disease initiation. It is a highly dynamic and multistep process that can be stimulated by various stimuli, including cellular stress, DNA damage, telomere shortening, and oncogene activation. Also, senescence is a potent antitumor mechanism, by preventing the proliferation of cancerous cells. However, some of the senescent cells have apoptosis resistance and can cause recurrence in cancer. A new class of drugs termed senolytics selectively kill and eliminate senescent cells. In recent years, natural compounds such as quercetin have been discovered to be effective as senolytic agents. Quercetin is a phytochemical that has strong antioxidant properties and pro-apoptotic effects and has been investigated for many years. Additionally, it has great potential to be used as a senolytic agent. According to preclinical and early-phase clinical data of senolytic agent research, quercetin administration appears to be effective in preventing or alleviating cancer formation. In this paper, we review the importance of cellular senescence in carcinogenesis and the effects of quercetin on senescence, as well as quercetin's potential effects as a pro-apoptotic agent and suppressor of cancer cell proliferation. (c) 2022 Elsevier Inc. All rights reserved.
dc.titleEnglish
dc.typeONCOGENE-INDUCED SENESCENCE
dc.typeCELLULAR SENESCENCE
dc.typeCANCER
dc.typeAPOPTOSIS
dc.typeCELLS
dc.typeCYCLE
dc.typePROLIFERATION
dc.typeEXPRESSION
dc.typeCARCINOMA
dc.typeRELEASE

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