{"doi":"10.3390/ijms27010357","title":"Therapy-Induced Senescence (TIS) and SASP: The p53-Mediated Interplay in Cancer Progression and Treatment","abstract":"<jats:p>Cellular senescence, initially regarded as a potent tumor-suppressive mechanism, is now recognized as a double-edged sword that modulates the hallmarks of cancer. The tumor suppressor p53 typically orchestrates this process to inhibit tumorigenesis; however, mutations in p53 or its regulators can subvert this program, leading to senescence evasion and therapy resistance. In particular, therapy-induced senescence can paradoxically drive tumor progression via the senescence-associated secretory phenotype, which creates a pro-tumorigenic microenvironment dictated by p53-mediated regulation of NF-κB signaling. Here, we explore the p53-mediated senescence–cancer interplay and evaluate emerging therapies, including senolytics and immunotherapies. We propose that strategic modulation of senescence offers a promising paradigm for future anticancer therapy.</jats:p>","journal":"International Journal of Molecular Sciences","year":2025,"id":625561,"datarank":0.29188652235829704,"base_score":1.9459101490553132,"endowment":1.9459101490553132,"self_citation_contribution":0.29188652235829704,"citation_network_contribution":0.0,"self_endowment_contribution":0.29188652235829704,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":6,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1617874,"name":"Tuan Minh Nguyen","orcid":"0000-0001-6215-8266","position":1,"is_corresponding":false},{"id":1617875,"name":"Yongook Lee","orcid":null,"position":2,"is_corresponding":false},{"id":1617876,"name":"Seoung Gyu Choi","orcid":null,"position":3,"is_corresponding":false},{"id":1617877,"name":"Phuong Ngan Nguyen","orcid":null,"position":4,"is_corresponding":false},{"id":153499,"name":"Jung Ho Park","orcid":"0000-0002-8367-4371","position":5,"is_corresponding":false},{"id":623230,"name":"Mi Kyung Park","orcid":"0000-0003-4257-6799","position":6,"is_corresponding":false},{"id":193322,"name":"Chang Hoon Lee","orcid":"0000-0003-2210-0793","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Therapy-Induced Senescence (TIS) and SASP: The p53-Mediated Interplay in Cancer Progression and Treatment","abstract":"<jats:p>Cellular senescence, initially regarded as a potent tumor-suppressive mechanism, is now recognized as a double-edged sword that modulates the hallmarks of cancer. The tumor suppressor p53 typically orchestrates this process to inhibit tumorigenesis; however, mutations in p53 or its regulators can subvert this program, leading to senescence evasion and therapy resistance. In particular, therapy-induced senescence can paradoxically drive tumor progression via the senescence-associated secretory phenotype, which creates a pro-tumorigenic microenvironment dictated by p53-mediated regulation of NF-κB signaling. Here, we explore the p53-mediated senescence–cancer interplay and evaluate emerging therapies, including senolytics and immunotherapies. 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