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二甲双胍对抗乳腺癌化疗耐药性:靶向癌症干细胞

Counteracting Chemoresistance with Metformin in Breast Cancers: Targeting Cancer Stem Cells.

作者信息

Samuel Samson Mathews, Varghese Elizabeth, Koklesová Lenka, Líšková Alena, Kubatka Peter, Büsselberg Dietrich

机构信息

Department of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, Doha 24144, Qatar.

Department of Obstetrics and Gynecology, Jessenius Faculty of Medicine, Comenius University in Bratislava, 03601 Martin, Slovakia.

出版信息

Cancers (Basel). 2020 Sep 1;12(9):2482. doi: 10.3390/cancers12092482.

Abstract

Despite the leaps and bounds in achieving success in the management and treatment of breast cancers through surgery, chemotherapy, and radiotherapy, breast cancer remains the most frequently occurring cancer in women and the most common cause of cancer-related deaths among women. Systemic therapeutic approaches, such as chemotherapy, although beneficial in treating and curing breast cancer subjects with localized breast tumors, tend to fail in metastatic cases of the disease due to (a) an acquired resistance to the chemotherapeutic drug and (b) the development of intrinsic resistance to therapy. The existence of cancer stem cells (CSCs) plays a crucial role in both acquired and intrinsic chemoresistance. CSCs are less abundant than terminally differentiated cancer cells and confer chemoresistance through a unique altered metabolism and capability to evade the immune response system. Furthermore, CSCs possess active DNA repair systems, transporters that support multidrug resistance (MDR), advanced detoxification processes, and the ability to self-renew and differentiate into tumor progenitor cells, thereby supporting cancer invasion, metastasis, and recurrence/relapse. Hence, current research is focusing on targeting CSCs to overcome resistance and improve the efficacy of the treatment and management of breast cancer. Studies revealed that metformin (1, 1-dimethylbiguanide), a widely used anti-hyperglycemic agent, sensitizes tumor response to various chemotherapeutic drugs. Metformin selectively targets CSCs and improves the hypoxic microenvironment, suppresses the tumor metastasis and inflammation, as well as regulates the metabolic programming, induces apoptosis, and reverses epithelial-mesenchymal transition and MDR. Here, we discuss cancer (breast cancer) and chemoresistance, the molecular mechanisms of chemoresistance in breast cancers, and metformin as a chemo-sensitizing/re-sensitizing agent, with a particular focus on breast CSCs as a critical contributing factor to acquired and intrinsic chemoresistance. The review outlines the prospects and directions for a better understanding and re-purposing of metformin as an anti-cancer/chemo-sensitizing drug in the treatment of breast cancer. It intends to provide a rationale for the use of metformin as a combinatory therapy in a clinical setting.

摘要

尽管通过手术、化疗和放疗在乳腺癌的管理和治疗方面取得了长足的进展,但乳腺癌仍然是女性中最常见的癌症,也是女性癌症相关死亡的最常见原因。全身治疗方法,如化疗,虽然有助于治疗和治愈患有局限性乳腺肿瘤的乳腺癌患者,但在该疾病的转移病例中往往会失败,原因如下:(a)对化疗药物产生获得性耐药;(b)对治疗产生内在耐药性。癌症干细胞(CSC)的存在在获得性和内在化学抗性中都起着关键作用。CSC比终末分化的癌细胞数量少,并通过独特的代谢改变和逃避免疫反应系统的能力赋予化学抗性。此外,CSC拥有活跃的DNA修复系统、支持多药耐药(MDR)的转运蛋白、先进的解毒过程,以及自我更新和分化为肿瘤祖细胞的能力,从而促进癌症的侵袭、转移和复发/再发。因此,目前的研究集中在靶向CSC以克服耐药性,并提高乳腺癌治疗和管理的疗效。研究表明,二甲双胍(1,1-二甲基双胍),一种广泛使用的抗高血糖药物,可使肿瘤对各种化疗药物敏感。二甲双胍选择性地靶向CSC并改善缺氧微环境,抑制肿瘤转移和炎症,以及调节代谢程序,诱导细胞凋亡,并逆转上皮-间质转化和MDR。在此,我们讨论癌症(乳腺癌)和化学抗性、乳腺癌化学抗性的分子机制,以及二甲双胍作为化学增敏/再增敏剂,特别关注乳腺CSC作为获得性和内在化学抗性的关键促成因素。该综述概述了更好地理解和重新利用二甲双胍作为抗癌/化学增敏药物治疗乳腺癌的前景和方向。它旨在为在临床环境中使用二甲双胍作为联合治疗提供理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cd2/7565921/761004cc292a/cancers-12-02482-g001.jpg

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