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dc.contributor.authorSilva, Andrew Oliveirapt_BR
dc.contributor.authorBitencourt, Thais Cardosopt_BR
dc.contributor.authorVargas, José Eduardopt_BR
dc.contributor.authorFraga, Lucas Rosapt_BR
dc.contributor.authorChiela, Eduardo Cremonese Filippipt_BR
dc.date.accessioned2024-11-22T06:55:12Zpt_BR
dc.date.issued2024pt_BR
dc.identifier.issn1415-4757pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/281360pt_BR
dc.description.abstractSenescence is a cellular state in which the cell loses its proliferative capacity, often irreversibly. Physiologically, it occurs due to a limited capacity of cell division associated with telomere shortening, the so-called replicative senescence. It can also be induced early due to DNA damage, oncogenic activation, oxidative stress, or damage to other cellular components (collectively named induced senescence). Tumor cells acquire the ability to bypass replicative senescence, thus ensuring the replicative immortality, a hallmark of cancer. Many anti-cancer therapies, however, can lead tumor cells to induced senescence. Initially, this response leads to a slowdown in tumor growth. However, the longstanding accumulation of senescent cells (SnCs) in tumors can promote neoplastic progression due to the enrichment of numerous molecules and extracellular vesicles that constitutes the senescence-associated secretory phenotype (SASP). Among other effects, SASP can potentiate or unlock the tumor plasticity and phenotypic transitions, another hallmark of cancer. This review discusses how SnCs can fuel mechanisms that underlie cancer plasticity, like cell differentiation, stemness, reprogramming, and epithelial-mesenchymal transition. We also discuss the main molecular mechanisms that make SnCs resistant to cell death, and potential strategies to target SnCs. At the end, we raise open questions and clinically relevant perspectives in the field.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofGenetics and molecular biology. Ribeirão Preto, SP. Vol. 47, suppl. 1 (2024), e20230311, 18 p.pt_BR
dc.rightsOpen Accessen
dc.subjectNeoplasiaspt_BR
dc.subjectAgingen
dc.subjectCanceren
dc.subjectMicroambiente tumoralpt_BR
dc.subjectTumor microenvironmenten
dc.subjectEnvelhecimentopt_BR
dc.subjectPlasticityen
dc.subjectPlasticidade celularpt_BR
dc.subjectSenotherapyen
dc.titleModulation of tumor plasticity by senescent cells : deciphering basic mechanisms and survival pathways to unravel therapeutic optionspt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001209439pt_BR
dc.type.originNacionalpt_BR


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