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Mendelian randomization using UK Biobank and FinnGen data, alongside in vitro and in vivo models, evaluates effects on tumor immune checkpoint regulation. Statin-related HMGCR inhibition shows breast cancer risk reduction, and lovastatin suppresses paclitaxel-induced PD-L1 while strengthening CD8+ T-cell cytotoxicity.",{"@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/research-report/","Research & 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was the objective of this study?","Question",{"text":63,"@type":64},"To assess the relationship between statin use and cancer risk, and to investigate the potential role of statins in adjuvant treatment of breast cancer.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"What methods were used to evaluate statins and cancer risk?",{"text":68,"@type":64},"Mendelian randomization data were derived from genome-wide association studies in the UK Biobank and FinnGen, and statin and chemotherapy impacts were tested using in vitro and in vivo models.",{"name":70,"@type":61,"acceptedAnswer":71},"How did lovastatin affect paclitaxel-induced PD-L1 and immune responses?",{"text":72,"@type":64},"In vitro, lovastatin inhibited paclitaxel-induced PD-L1 expression and supported paclitaxel in suppressing tumor growth, while combination therapy increased CD8+ T-cell infiltration and enhanced tumor-killing capacity in 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cytotoxicity for better prognosis in breast cancer  \nLei Li, PhDa,c , Hongbin Wang, MDb , Shiyuan Zhang, MDb , Song Gao, MDb , Xiuxin Lu, MScb , You Pan, MDa , Wei Tang, MSca , Rong Huang, MSca , Kun Qiao, MDb,*, Shipeng Ning, MDa,*  \nBackground: In recent years, the widespread use of lipid-lowering drugs, especially statins, has attracted people ’s attention. Statin use may be potentially associated with a reduced risk of breast cancer.  \nObjective: To explore the relationship between statin use and cancer risk. And further explore the potential role of statins in theadjuvant treatment of breast cancer.  \nMethods: Data for the Mendelian randomization portion of the study were obtained from genome-wide association studies of common cancers in the UK Biobank and FinnGen studies and from the Global Lipid Genetics Consortium’s low density lipoprotein (LDL) . In addition, the impacts of statins and chemotherapy drugs on breast cancer were examined using both in vitro and in vivo models, with particular attention to the expression levels of the immune checkpoint protein PD-L1 and its potential to suppress tumor growth. Results: Data from about 3 .8 million cancer patients and ~1 .3 million LDL-measuring individuals were analyzed. Genetically proxied HMGCR inhibition (statins) was associated with breast cancer risk reduction (P = 0.0005) . In vitro experiments showed that lovastatinsignificantly inhibited paclitaxel-induced PD-L1 expression and assisted paclitaxel in suppressing tumor cell growth. Furthermore, the combination therapy involving lovastatin and paclitaxel amplified CD8 + T-cell infiltration, bolstering their tumor-killing capacity and enhancing in vivo efficacy.  \nConclusion: The utilization of statins is correlated with improved prognoses for breast cancer patients and may play a role in facilitating the transition from cold to hot tumors. Combination therapy with lovastatin and paclitaxel enhances CD8 + T-cell activity and leads to better prognostic characteristics.  \nKeywords: breast cancer, combination therapy, paclitaxel, PD-L1, statins  \nIntroduction  \nCancer stands as a prominent contributor to global mortality[1] . In 2018, the United States witnessed 609 640 deaths due to  \naDepartment of Breast Surgery, The Second Affiliated Hospital of Guangxi Medical University, Nanning, bDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, People ’s Republic of China and cDepartment of Pathology, University of Otago, Dunedin, New Zealand  \nLei Li and Hongbin Wang have contributed equally to this work and share first authorship.  \nSponsorships or competing interests that maybe relevant to content are disclosed atthe end of this article.  \n*Corresponding authors. Address. Department of breast surgery, Harbin medical university cancer hospital, Harbin 150000, China. Tel.: +451 862 98053. [E-mail: qiaokun@hrbmu.edu.cn](E-mail: qiaokun@hrbmu.edu.cn) (K. Qiao); Department of breast surgery,The Second Affiliated Hospital of Guangxi Medical University, Nanning 530000, China.  \nTel.: +771 327 [7533. E-mail: nspdoctor@sr.gxmu.edu.cn](7533. E-mail: nspdoctor@sr.gxmu.edu.cn) (S. Ning).  \nCopyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. This is an open access article distributed under the Creative Commons Attribution-ShareAlike License 4.0, which allows others to remix, tweak, and build upon the work, even for commercial purposes, as long as the author is credited and the new creations are licensed under the identical terms.  \nInternational Journal of Surgery (2024) 110:4716–4726  \nReceived 22 February 2024; Accepted 25 April 2024  \nSupplemental Digital Content is available for this article. Direct URL citations are provided in the HTML and PDF versions of this article on the journal's website, [www.lww.com/international-journal-of-surgery](www.lww.com/international-journal-of-surgery).  \nPubli","cbCailAe0nUtBYD9","https://ap.wps.com/l/cbCailAe0nUtBYD9","pdf",2367389,11,"English","# Background\n# Objective\n# Methods\n## Mendelian randomization and models\n## PD-L1 and immune effects\n# Results\n# Conclusion\n# Keywords","[{\"question\":\"What was the objective of this study?\",\"answer\":\"To assess the relationship between statin use and cancer risk, and to investigate the potential role of statins in adjuvant treatment of breast cancer.\"},{\"question\":\"What methods were used to evaluate statins and cancer risk?\",\"answer\":\"Mendelian randomization data were derived from genome-wide association studies in the UK Biobank and FinnGen, and statin and chemotherapy impacts were tested using in vitro and in vivo models.\"},{\"question\":\"How did lovastatin affect paclitaxel-induced PD-L1 and immune responses?\",\"answer\":\"In vitro, lovastatin inhibited paclitaxel-induced PD-L1 expression and supported paclitaxel in suppressing tumor growth, while combination therapy increased CD8+ T-cell infiltration and enhanced tumor-killing capacity in vivo.\"}]","Statins inhibit paclitaxel-induced PD-L1 expression and increase CD8+ T cytotoxicity for better prognosis in breast cancer | PDF",1789980119,28]