Abstract
To date, the tumor microenvironment (TME) has gained considerable attention in various areas of cancer research due to its role in driving a loss of immune surveillance and enabling rapid advanced tumor development and progression. The TME plays an integral role in driving advanced aggressive breast cancers, including triple-negative breast cancer (TNBC), a pivotal mediator for tumor cells to communicate with the surrounding cells via lymphatic and circulatory systems. Furthermore, the TME plays a significant role in all steps and stages of carcinogenesis by promoting and stimulating uncontrolled cell proliferation and protecting tumor cells from the immune system. Various cellular components of the TME work together to drive cancer processes, some of which include tumor-associated adipocytes, fibroblasts, macrophages, and neutrophils which sustain perpetual amplification and release of pro-inflammatory molecules such as cytokines. Thymoquinone (TQ), a natural chemical component from black cumin seed, is widely used traditionally and now in clinical trials for the treatment/prevention of multiple types of cancer, showing a potential to mitigate components of TME at various stages by various pathways. In this review, we focus on the role of TME in TNBC cancer progression and the effect of TQ on the TME, emphasizing their anticipated role in the prevention and treatment of TNBC. It was concluded from this review that the multiple components of the TME serve as a critical part of TNBC tumor promotion and stimulation of uncontrolled cell proliferation. Meanwhile, TQ could be a crucial compound in the prevention and progression of TNBC therapy through the modulation of the TME.
Highlights
Breast cancer (BC) is one of the most life-threatening diseases with the highest number of human cancer subtypes and is the second leading cause of death in women [1]
Similar studies have reported that reactive oxygen species (ROS) activates the antitumor activities of doxorubicin, resulting in the efficient inhibition of distant metastasis and tumor growth in Triple-negative breast cancer (TNBC) cells [86]
This review focuses on the roles of tumorassociated macrophage (TAM), cancer-associated adipocytes (CAAs), cancer-associated fibroblasts (CAFs), tumor-infiltrating lymphocytes (TILs), Il6, and transforming growth factor-β (TGF-β) in the tumor microenvironment (TME)
Summary
Breast cancer (BC) is one of the most life-threatening diseases with the highest number of human cancer subtypes and is the second leading cause of death in women [1]. Triple-negative breast cancer (TNBC) is characterized by a lack of expressed progesterone receptors, estrogen receptors, and human epidermal growth factor 2 (HER2) [4] It is one of the major metastatic, drug-resistant, and aggressive sub-classes of BC [5], which comprises around 20% of total BC globally [6], and 83% of deaths compared with other BC subtypes [7]. The most indispensable is the TME, directly linked with angiogenesis, rapid cell proliferation, immune system suppression, apoptosis inhibition, and eventual evasion of immune surveillance in the tumor area [8] Because of these activities, TME can be noted as a critical hallmark in cancer pathogenicity and a potential target for TNBC [9].
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