Therapeutic Implications of the Drug Resistance Conferred by Extracellular Vesicles Derived from Triple-Negative Breast Cancer Cells

Abstract

Anticancer drug resistance is a significant impediment in current cancer treatment. Extracellular vesicles (EVs) derived from cancer cells were recently acknowledged as a critical mechanism of drug resistance, tumor progression, and metastasis. EVs are enveloped vesicles comprising a lipid bilayer that transfers various cargo, including proteins, nucleic acids, lipids, and metabolites, from an originating cell to a recipient cell. Investigating the mechanisms whereby EVs confer drug resistance is still in the early stages. In this review, I analyze the roles of EVs derived from triple-negative breast cancer cells (TNBC-EVs) in anticancer drug resistance and discuss strategies to overcome TNBC-EV-mediated drug resistance.

Identification of exosome-related gene signature as a promising diagnostic and therapeutic tool for breast cancer

“…Exosomes play a significant role in transferring information and signaling molecules between cells, thereby activating pathways that promote cell proliferation, angiogenesis, and immune evasion, while also suppressing antitumor immune responses [ [10] , [11] , [12] ]. Specifically, exosomes from stromal or cancer cells within the tumor microenvironment (TME) are crucial in drug resistance development [ 13 , 14 ]. By transferring signaling molecules like miRNAs, proteins, and transcription factors [ 15 ], these vesicles can alter gene expression in recipient cells and induce drug resistance.…”

“…Infiltrating immune cells within the TME modulate immune responses and promote tumor cell migration and invasion [ 14 ]. This process contributes to the formation of premetastatic niches in distant organs for disseminated tumor cells [ 14 ].…”

“…Infiltrating immune cells within the TME modulate immune responses and promote tumor cell migration and invasion [ 14 ]. This process contributes to the formation of premetastatic niches in distant organs for disseminated tumor cells [ 14 ]. These cells exert antitumor effects by releasing cytotoxic substances, recognizing and eliminating tumor cells, and producing cytokines [ 20 , 21 ].…”

Mitochondria Targeted AuCu@Ce6-TPP nanoparticles Alleviating Cancer Hypoxia for Enhanced Photodynamic Therapy

“…As the most prevalent cancer in the globe, breast cancer accounts for approximately 30% of female malignancies and is the primary cause of cancer-related mortality among women aged 20 to 59 3,4 . One typical feature of intractable triple-negative breast cancers (TNBC) is the hypoxic microenvironment, which provides tumor cells with unique capabilities to resist diverse forms of anticancer therapies, including photodynamic therapy (PDT), chemotherapy, immunotherapy, and radiation therapy [5][6][7] .…”

Novel Therapeutic Targets in Cancers

“…However, EVs can also contribute to cancer development and progression by promoting drug resistance; consequently, they can facilitate tumor growth and spread. The paper by Yi et al [12] provides an informative synopsis of the oncogenic signaling mediated by EVs derived from cancer cells and their potential as a novel target for anti-cancer therapy. In this review, they also point out the obstacles of this approach: the heterogeneity of EVs, the lack of specific markers, and the difficulty of isolating and characterizing them.…”