Metformin boosts doxorubicin efficacy and increases CD8 + T cell frequency in mouse breast cancer.

IF 2.8 3区医学 Q2 ONCOLOGY

Clinical & Translational Oncology Pub Date : 2024-10-29 DOI:10.1007/s12094-024-03764-2

Elaheh Hassani, Sahand Mozzendizaji, Vahid Shafiei-Irannejad, Adel Mohammadzadeh

{"title":"Metformin boosts doxorubicin efficacy and increases CD8 + T cell frequency in mouse breast cancer.","authors":"Elaheh Hassani, Sahand Mozzendizaji, Vahid Shafiei-Irannejad, Adel Mohammadzadeh","doi":"10.1007/s12094-024-03764-2","DOIUrl":null,"url":null,"abstract":"Purpose: Breast cancer is a leading cause of cancer-related deaths among women worldwide. The presence and function of CD8 + T cells in the tumor microenvironment have been associated with better patient outcomes. Drug toxicity has posed a significant challenge to the clinical implementation of chemotherapy-based strategies in cancer treatment.Methods: In this study, we employed flow cytometry to investigate the potential synergistic immunomodulatory effects on CD8 + T cells in a mouse model of breast cancer by combining metformin, an anti-diabetic medication, with doxorubicin.Results: Through flow cytometry analysis, we observed that the combination of the two drugs led to an increased percentage of CD8 + T cells compared to either drug alone. The modulation of HIF-1α and STAT3 gene expression in the combination group further confirmed the efficacy of this approach.Conclusions: Our findings suggest that combining metformin with doxorubicin can enhance the anticancer activity of doxorubicin and decrease its cytotoxicity in a 4T1 breast cancer mouse model.","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":null,"pages":null},"PeriodicalIF":2.8000,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical & Translational Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12094-024-03764-2","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Purpose: Breast cancer is a leading cause of cancer-related deaths among women worldwide. The presence and function of CD8 + T cells in the tumor microenvironment have been associated with better patient outcomes. Drug toxicity has posed a significant challenge to the clinical implementation of chemotherapy-based strategies in cancer treatment.

Methods: In this study, we employed flow cytometry to investigate the potential synergistic immunomodulatory effects on CD8 + T cells in a mouse model of breast cancer by combining metformin, an anti-diabetic medication, with doxorubicin.

Results: Through flow cytometry analysis, we observed that the combination of the two drugs led to an increased percentage of CD8 + T cells compared to either drug alone. The modulation of HIF-1α and STAT3 gene expression in the combination group further confirmed the efficacy of this approach.

Conclusions: Our findings suggest that combining metformin with doxorubicin can enhance the anticancer activity of doxorubicin and decrease its cytotoxicity in a 4T1 breast cancer mouse model.

查看原文本刊更多论文

二甲双胍提高了多柔比星的疗效，并增加了小鼠乳腺癌 CD8 + T 细胞的频率。

目的：乳腺癌是全球妇女因癌症死亡的主要原因。肿瘤微环境中 CD8 + T 细胞的存在和功能与更好的患者预后有关。药物毒性对基于化疗的癌症治疗策略的临床实施构成了重大挑战：在这项研究中，我们采用流式细胞术研究了抗糖尿病药物二甲双胍与多柔比星联合使用对乳腺癌小鼠模型中 CD8 + T 细胞的潜在协同免疫调节作用：结果：通过流式细胞术分析，我们观察到与单独使用两种药物相比，联合使用两种药物可增加 CD8 + T 细胞的比例。联合用药组中 HIF-1α 和 STAT3 基因表达的调节进一步证实了这种方法的有效性：我们的研究结果表明，在4T1乳腺癌小鼠模型中，二甲双胍与多柔比星联用可增强多柔比星的抗癌活性并降低其细胞毒性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Clinical & Translational Oncology 医学-肿瘤学

CiteScore

6.20

自引率

2.90%

发文量

240

审稿时长

1 months

期刊介绍： Clinical and Translational Oncology is an international journal devoted to fostering interaction between experimental and clinical oncology. It covers all aspects of research on cancer, from the more basic discoveries dealing with both cell and molecular biology of tumour cells, to the most advanced clinical assays of conventional and new drugs. In addition, the journal has a strong commitment to facilitating the transfer of knowledge from the basic laboratory to the clinical practice, with the publication of educational series devoted to closing the gap between molecular and clinical oncologists. Molecular biology of tumours, identification of new targets for cancer therapy, and new technologies for research and treatment of cancer are the major themes covered by the educational series. Full research articles on a broad spectrum of subjects, including the molecular and cellular bases of disease, aetiology, pathophysiology, pathology, epidemiology, clinical features, and the diagnosis, prognosis and treatment of cancer, will be considered for publication.