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Because S6K1 mainly regulates translation, this study aimed to define its pivotal roles in translational control and to discover novel targets in breast cancer cells. Ribosome profiling (Ribo-seq), RNA sequencing, and mass spectrometry identified CLU as a key autophagy-related target. Western blotting, immunofluorescence, and bafilomycin A1 experiments showed S6K1 modulates CLU translation to promote autophagosome formation.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/s6k1-overexpression-enhances-autophagy-in-breast-cancer-cells-by-inducing-the-translation-of-clu/373977/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/s6k1-overexpression-enhances-autophagy-in-breast-cancer-cells-by-inducing-the-translation-of-clu/373977.png","ImageObject",300,407,{"name":92,"@type":93},"MrHarris58","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-03","2026-09-23",true,{"@type":102,"interactionType":103,"userInteractionCount":44},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"Why is S6K1 important in breast cancer?","Question",{"text":112,"@type":113},"S6K1 is often amplified in breast cancer and correlates with drug resistance and poor prognosis. It is mainly involved in regulating translation processes.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How did the study identify CLU as a target of S6K1?",{"text":117,"@type":113},"The study used ribosome profiling (Ribo-seq) with integrated multiomics analyses including RNA sequencing and mass spectrometry. It then confirmed S6K1-dependent CLU translation with Western blotting and immunofluorescence.",{"name":119,"@type":110,"acceptedAnswer":120},"What is the relationship between S6K1 and autophagy in breast cancer cells?",{"text":121,"@type":113},"S6K1 depletion reduced global mRNA translation and prominently affected autophagy-related pathways. S6K1 overexpression increased CLU translation and facilitated autophagosome formation, supporting that S6K1 promotes autophagy through CLU.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},373977,1791457243,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":44,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},687212988360,"https://ap-avatar.wpscdn.com/davatar_276721f389ce27ea32af1340a28f341c","Original Article  \nS6K1 overexpression enhances autophagy in breast cancer cells by inducing the translation of CLU  \nXingmei Shu1, Ranjiaxi Wang1, Yan Liu1,2, Xiaoqian Shi1, Yuhao Liu1, Yinan Chen1, Jinming Shi1, Mingyang Liu1, Yongmei Song1, Dan Li1,3  \n1State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China;  \n2Institute of Cancer Stem Cell, Dalian Medical University, Dalian, Liaoning 116051, China;  \n3Laboratory Animal Center, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.  \nAbstract  \nBackground: Ribosomal protein S6 kinase B1 (S6K1) is frequently amplified and correlates with drug resistance and poor prognosis in patients with breast cancer. Although S6K1 functions primarily in the process of translation, the genome-wide translational profiles regulated by S6K1 remain unclear. This study sought to clarify the pivotal role of S6K1 in translational regulation and investigate its novel targets in breast cancer.  \nMethods: Ribosome profiling sequencing (Ribo-seq) was performed to explore genome-wide translational profiles regulated by S6K1 in breast cancer cells. Integrated multiomics analyses, including Ribo-seq, RNA sequencing, and mass spectrometry, were employed to identify a new target of S6K1 translational regulation, the autophagy-related gene clusterin ( CLU). Western blotting and immunofluorescence were utilized to confirm that S6K1 regulated CLU translation, thus influencing autophagy in breast cancer cells. Bafilomycin A1 (a late-stage autophagy inhibitor) was used to demonstrate that S6K1 regulated autophagosome formation in breast cancer cells through affecting the translation of CLU.  \nResults: S6K1 depletion resulted in the downregulation of global messenger RNA (mRNA) translation and affected translation in multiple pathways that play crucial roles in carcinogenesis, with autophagy-related pathways being the most prominently affected. The role of S6K1 in autophagy was further confirmed in breast cancer cells, and CLU was identified as a novel target regulated by S6K1 at the translational level. Additionally, the overexpression of S6K1 promoted the translation of CLU, thus facilitating the formation of autophagosomes.  \nConclusion: This study demonstrated that the overexpression of S6K1 promoted autophagy in breast cancer cells by facilitating the translation of the autophagy-related gene CLU.  \nKeywords: Ribosome profiling sequencing; Ribosomal protein S6 kinase B1; CLU; Autophagy; Breast cancer  \nIntroduction  \nBreast cancer is a widespread and significant health concern globally, with increasing incidence rates and burdens on healthcare systems. [1] In China, breast cancer accounts for 15.59% of newly diagnosed cancer cases and approximately 7.94% of deaths each year. [2] Our previous study revealed that certain patients with estrogen receptorpositive (ER+), human epidermal growth factor receptor 2-negative (HER2−) breast cancer exhibited resistance to cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors due to amplification of the ribosomal protein S6 kinase B1 (RPS6KB1 ) gene. The overexpression of ribosomal  \n\n| Access this article online |  |\n| --- | --- |\n| Quick Response Code: | Website:\u003Cbr>[www.cmj.org](www.cmj.org) |\n|  | DOI:\u003Cbr>10.1097/CM9.0000000000003596 |\n\nprotein S6 kinase 1 (S6K1, encoded by RPS6KB1 ) activated the translation of the MYC proto-oncogene, bHLH transcription factor (c-Myc),[3] thus accelerating the G1/S transition and ultimately resulting in resistance to CDK4/6 inhibitors. [4] Moreover, S6K1 amplification has been identified in various other cancer types, including stomach adenocarcinoma, uterine carcinosarcoma, and esophageal adenocarcinoma,[4] and has been reported to be associated wit","cbCainLGZbAmzVEi","https://ap.wps.com/l/cbCainLGZbAmzVEi","pdf",25923110,13,"English","# Abstract\n## Background\n## Methods\n## Results\n## Conclusion\n# Introduction","[{\"question\":\"Why is S6K1 important in breast cancer?\",\"answer\":\"S6K1 is often amplified in breast cancer and correlates with drug resistance and poor prognosis. It is mainly involved in regulating translation processes.\"},{\"question\":\"How did the study identify CLU as a target of S6K1?\",\"answer\":\"The study used ribosome profiling (Ribo-seq) with integrated multiomics analyses including RNA sequencing and mass spectrometry. It then confirmed S6K1-dependent CLU translation with Western blotting and immunofluorescence.\"},{\"question\":\"What is the relationship between S6K1 and autophagy in breast cancer cells?\",\"answer\":\"S6K1 depletion reduced global mRNA translation and prominently affected autophagy-related pathways. S6K1 overexpression increased CLU translation and facilitated autophagosome formation, supporting that S6K1 promotes autophagy through CLU.\"}]","S6K1 overexpression enhances autophagy in breast cancer cells by inducing the translation of CLU | PDF",1790200934,33]