[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-339980-105":3,"detail-sidebar-cat-0-en-105":81,"doc-detail-339980-en":130},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":74,"head_meta":76,"extra_data":78,"updated_unix":80},105,"en","cellular-senescence-and-sasp-in-tumor-progression-and-therapeutic-opportunities","Cellular senescence and SASP in tumor progression and therapeutic opportunities","","Cellular senescence (CS) is a permanent cell-cycle arrest that contributes to major physiological and pathological processes, especially cancer. Although CS was first viewed as a barrier to tumorigenesis, accumulating evidence shows senescent cells can accelerate tumor progression through senescence-associated secretory phenotypes (SASPs). SASPs remodel the tumor microenvironment (TME) by altering immune responses and stromal signaling, yet may also enhance immunosurveillance in some contexts. The review summarizes CS and SASP roles and therapeutic strategies using senolytics and senomorphics to clear senescent cells or reduce SASP damage.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/cellular-senescence-and-sasp-in-tumor-progression-and-therapeutic-opportunities/339980/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/cellular-senescence-and-sasp-in-tumor-progression-and-therapeutic-opportunities/339980.png","ImageObject",300,407,{"name":42,"@type":43},"Levi","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-29","2026-09-21",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",19,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"What is cellular senescence (CS) and why is it important in cancer?","Question",{"text":63,"@type":64},"CS is a permanent arrest of the cell cycle and proliferation. It is implicated in cancer because senescent cells can influence tumor development through their secretory behavior.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How do SASPs contribute to tumor progression?",{"text":68,"@type":64},"SASPs include chemokines, growth factors, cytokines, and matrix-related proteases that reshape the tumor microenvironment (TME). This can help tumors evade immune destruction and alter stromal signaling.",{"name":70,"@type":61,"acceptedAnswer":71},"Why is SASP described as having a “double-edged sword” role?",{"text":72,"@type":64},"The review notes that SASPs may promote tumor progression in many settings, but some studies suggest they can also impede tumor development by enhancing immunosurveillance. This reflects heterogeneity across cancers and contexts.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},339980,1790040254,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,110,115,120,123,127],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":102,"doc_module":4,"doc_module_name":25,"category_name":103,"show_sort_weight":104,"slug":105},6,"Technology",50,"technology",{"id":107,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":108,"slug":109},7,40,"healthcare",{"id":111,"doc_module":4,"doc_module_name":25,"category_name":112,"show_sort_weight":113,"slug":114},8,"Research & Report",30,"research-report",{"id":116,"doc_module":4,"doc_module_name":25,"category_name":117,"show_sort_weight":118,"slug":119},9,"Religion & Spirituality",20,"religion-spirituality",{"id":118,"doc_module":4,"doc_module_name":25,"category_name":121,"show_sort_weight":118,"slug":122},"World Cup","world-cup",{"id":124,"doc_module":4,"doc_module_name":25,"category_name":125,"show_sort_weight":124,"slug":126},10,"Lifestyle","lifestyle",{"id":55,"doc_module":4,"doc_module_name":25,"category_name":128,"show_sort_weight":97,"slug":129},"General","general",{"code":4,"msg":82,"data":131},{"doc_id":79,"user_id":132,"nickname":42,"user_avatar":133,"doc_module":4,"category_id":107,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":55,"language":139,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":12,"update_tm":143,"read_time":144},7971461740909,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","Dong et al. Molecular Cancer (2024) 23:181 [https://doi.org/10.1186/s12943-024-02096-7](https://doi.org/10.1186/s12943-024-02096-7)  \nMolecular Cancer  \n REVIEW Open Access  \nCellular senescence and SASP in tumor progression and therapeutic opportunities  \nZening Dong1†, Yahan Luo2†, Zhangchen Yuan1, Yu Tian1, Tianqiang Jin1* and Feng Xu1*  \nAbstract  \nCellular senescence (CS), a permanent and irreversible arrest of the cell cycle and proliferation leading to the degeneration of cellular structure and function, has been implicated in various key physiological and pathological processes, particularly in cancer. Initially, CS was recognized as a barrier to tumorigenesis, serving as an intrinsic defense mechanism to protect cells from malignant transformation. However, increasing evidence suggests that senescent cells can promote tumor progression to overt malignancy, primarily through a set offactors known as senescence-associated secretory phenotypes (SASPs), including chemokines, growth factors, cytokines, and stromal metalloproteinases. These factors significantly reshape the tumor microenvironment (TME), enabling tumors to evade immune destruction. Interestingly, some studies have also suggested that SASPs may impede tumor development by enhancing immunosurveillance. These opposing roles highlight the complexity and heterogeneity of CS and SASPs in diverse cancers. Consequently, there has been growing interest in pharmacological interventions targeting CS or SASPsin cancer therapy, such as senolytics and senomorphics, to either promote the clearance of senescent cells or mitigate the harmful effects of SASPs. In this review, we will interpret the concept of CS, delve into the role of SASPs in reshaping the TME, and summarize recent advances in anti-tumor strategies targeting CS or SASPs.  \nKeywords Cellular senescence, SASP, Tumor, Tumor microenvironment, Therapy  \nIntroduction  \nCellular senescence (CS) was initially introduced in 1961 [1]. In 1965, it was further described as a manifestation of the finite replicative capacity of diploid cell lines in vivo, characterized by the Hayflick limit, which represents the maximum number of cell divisions achievable before cellular growth arrest [2]. This phenomenon was subsequently defined as replicative senescence, which was  \n†Zening Dong andYahan Luo contributed equally to this work.  \n*Correspondence: Tianqiang Jin [jtq19950827@163.com](jtq19950827@163.com)[ ](jtq19950827@163.com)Feng Xu [fxu@cmu.edu.cn](fxu@cmu.edu.cn)  \n1 Hepatobiliary and Splenic Surgery Ward, Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, China  \n2 Shanghai TCM-Integrated Hospital, Shanghai University of TCM, Shanghai, China  \nconsidered irreversible and permanent due to the cell’sinability to physiologically reverse this cycle arrest [3]. Recent studies have shown that CS can result from exposure to various internal or external stressors, such as replication stress, telomere damage, metabolic disorders, and carcinogenic factors [4], leading to different types of senescence. In addition to arrested growth, another key feature of CS is the senescence-associated secretory phenotype (SASP), which includes a range of proinflammatory and proteolytic factors. SASP is generally diverse and dynamic, varying according to the type of senescent cells and the cellular environment [5]. However, SASP can also influence the surrounding environment, making CS and SASP not only cellular phenomena but also closely related to the development of various diseases, particularly tumors. For instance, SASP can either promote or inhibit tumor progression by remodeling the tumor microenvironment (TME), while the TME, in  \n© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give a","cbCaipozBQ1pYSha","https://ap.wps.com/l/cbCaipozBQ1pYSha","pdf",1615943,"English","# Abstract\n# Introduction\n# Types of CS\n## Replicative senescence\n# SASP and its impact on the tumor microenvironment\n# Anti-senescent therapies and therapeutic opportunities","[{\"question\":\"What is cellular senescence (CS) and why is it important in cancer?\",\"answer\":\"CS is a permanent arrest of the cell cycle and proliferation. It is implicated in cancer because senescent cells can influence tumor development through their secretory behavior.\"},{\"question\":\"How do SASPs contribute to tumor progression?\",\"answer\":\"SASPs include chemokines, growth factors, cytokines, and matrix-related proteases that reshape the tumor microenvironment (TME). This can help tumors evade immune destruction and alter stromal signaling.\"},{\"question\":\"Why is SASP described as having a “double-edged sword” role?\",\"answer\":\"The review notes that SASPs may promote tumor progression in many settings, but some studies suggest they can also impede tumor development by enhancing immunosurveillance. This reflects heterogeneity across cancers and contexts.\"}]","Cellular senescence and SASP in tumor progression and therapeutic opportunities | PDF",1790033500,48]