{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T17:57:30Z","timestamp":1790618250385,"version":"4.1.0"},"reference-count":219,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,9,13]],"date-time":"2026-09-13T00:00:00Z","timestamp":1789257600000},"content-version":"vor","delay-in-days":12,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Reports"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Cellular senescence influences cancer progression through irreversible cell\u2010cycle arrest, immune surveillance, and paracrine signaling mediated by the senescence\u2010associated secretory phenotype (SASP). SASP comprises inflammatory cytokines, chemokines, growth factors, and matrix\u2010remodeling enzymes that regulate the tumor microenvironment (TME).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This review describes the current evidence on the mechanisms of SASP induction, its condition\u2010dependent roles in cancer, TME remodeling, and emerging strategies targeting senescent cells and SASP signaling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Relevant literature was identified through searches on PubMed, Scopus, Web of Science, and Google Scholar using keywords related to cellular senescence, SASP, cancer, TME, senolytics, and senomorphics. Peer\u2010reviewed English\u2010language studies published primarily between January 2000\u2010 March 2026 were considered, including preclinical (in vitro, in\u00a0vivo), and clinical studies investigating SASP induction and regulation, its role in cancer progression and TME remodeling, and therapeutic strategies targeting senescent cells or SASP signaling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation of the Retrieved Articles<\/jats:title>\n                    <jats:p>SASP exhibits both tumor\u2010suppressive and tumor\u2010promoting activities depending on cellular and tissue condition. While transient SASP may enhance antitumor immunity and suppress early tumorigenesis, persistent SASP, particularly during therapy\u2010induced senescence (TIS), can promote tumor growth, angiogenesis, immune evasion, cancer stemness, metastasis, and therapeutic resistance. Senolytics and senomorphics have therefore emerged as promising approaches for targeting senescent cells and their detrimental secretory effects. SASP\u2010associated molecules also show potential as biomarkers, although specificity and tissue\u2010dependent heterogeneity remain major challenges.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Current evidence supports SASP as a major regulator of the TME and an important determinant of cancer progression and therapeutic response. Understanding the condition\u2010dependent functions of SASP is critical for developing effective senescence\u2010targeted cancer therapies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cnr2.70682","type":"journal-article","created":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T01:35:41Z","timestamp":1789349741000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["A Review of Senescence\u2010Associated Secretory Phenotype\u2010Mediated Remodeling of the Tumor Microenvironment: Implications for Cancer Progression and Therapy"],"prefix":"10.1002","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-5649-1597","authenticated-orcid":false,"given":"Sneha","family":"Pallatt","sequence":"first","affiliation":[{"name":"Medical Biotechnology Lab, Faculty of Allied and Healthcare Sciences Chettinad Academy of Research and Education (CARE), Chettinad Hospital and Research Institute (CHRI)  Chennai 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