{"title":"Vitexin Inhibits TNBC Progression and Metastasis by Modulating Macrophage Polarization Through EGFR Signaling.","authors":"Yufeng Lin, Lin Li, Huakang Huang, Xiaohong Wen, Yongcheng Zhang, Rongxin Zhang, Wenbin Huang","doi":"10.1097/CJI.0000000000000519","DOIUrl":null,"url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) lacks sensitivity to endocrine and targeted therapies, exhibiting high recurrence and poor prognosis postchemotherapy. Tumor-associated macrophages (TAMs) play a crucial role in cancer progression. Vitexin, a compound with diverse pharmacological effects including anti-cancer activity, remains unexplored in its impact on TAMs during TNBC development. This study aimed to investigate vitexin's effect on TNBC, its regulation of macrophage polarization (M1 vs. M2), and the underlying EGFR/PI3K/AKT/mTOR pathway. Our results demonstrated that vitexin suppressed the proliferation and invasion of TNBC cells (MDA-MB-231 and BT549) while inducing macrophage mediators that further inhibited cancer cell migration. Vitexin also promoted M1 polarization and suppressed M2 polarization, affecting EGFR phosphorylation and downstream signaling. In vivo, vitexin inhibited tumor growth, favoring M1 polarization and suppressing M2 polarization, with synergistic effects when combined with doxorubicin (Dox). These findings offer novel insights into vitexin's potential in TNBC treatment.</p>","PeriodicalId":15996,"journal":{"name":"Journal of Immunotherapy","volume":" ","pages":"303-312"},"PeriodicalIF":3.2000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Immunotherapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/CJI.0000000000000519","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/7 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Triple-negative breast cancer (TNBC) lacks sensitivity to endocrine and targeted therapies, exhibiting high recurrence and poor prognosis postchemotherapy. Tumor-associated macrophages (TAMs) play a crucial role in cancer progression. Vitexin, a compound with diverse pharmacological effects including anti-cancer activity, remains unexplored in its impact on TAMs during TNBC development. This study aimed to investigate vitexin's effect on TNBC, its regulation of macrophage polarization (M1 vs. M2), and the underlying EGFR/PI3K/AKT/mTOR pathway. Our results demonstrated that vitexin suppressed the proliferation and invasion of TNBC cells (MDA-MB-231 and BT549) while inducing macrophage mediators that further inhibited cancer cell migration. Vitexin also promoted M1 polarization and suppressed M2 polarization, affecting EGFR phosphorylation and downstream signaling. In vivo, vitexin inhibited tumor growth, favoring M1 polarization and suppressing M2 polarization, with synergistic effects when combined with doxorubicin (Dox). These findings offer novel insights into vitexin's potential in TNBC treatment.
期刊介绍:
Journal of Immunotherapy features rapid publication of articles on immunomodulators, lymphokines, antibodies, cells, and cell products in cancer biology and therapy. Laboratory and preclinical studies, as well as investigative clinical reports, are presented. The journal emphasizes basic mechanisms and methods for the rapid transfer of technology from the laboratory to the clinic. JIT contains full-length articles, review articles, and short communications.