Extracellular vesicles (EVs) are lipid-bilayer enclosed particles produced by all types of cells, and their roles as important couriers for intercellular communication have been gaining increasing amounts of appreciation. There are two major types of EVs classified based on their sizes and biogenesis, microvesicles (MVs) and exosomes. These vesicles contain specialized cargoes depending on their cellular origin, and they can induce phenotypic changes in recipient cells. The involvement of EVs in cancer is essential for disease progression. Specifically, EV-mediated communication between cancer cells and the other types of cells (i.e. endothelial cells, fibroblasts, immune cells, etc.) in the tumor microenvironment (TME) has been shown to promote cancer proliferation, survival, immune evasion, and invasion and metastasis. In chapter 2, I show that a highly aggressive triple-negative breast cancer (TNBC) cell line, MDA-MB-231 cells, produce EVs that can convert primary (non-immortalized) normal human dermal fibroblasts (NHDFs) into cancer-associated fibroblasts (CAFs), a phenotype found within the TME. CAFs are critical for reshaping the extracellular matrix to promote malignant transformation. I discovered this effect is driven by the fibronectin that coats the surfaces of these EVs, and its ability to engage the integrins expressed in the fibroblasts. This event then activates the focal adhesion kinase (FAK), phosphoinositide 3-kinase (PI3K), and AKT signaling pathway, which results in the inactivation of glycogen synthase kinase-3 $\beta$ (GSK3-$\beta$) and CAF formation. I also discovered tubulointerstitial nephritis antigen-like 1 (TINAGL1) is expressed on the surfaces of exosomes produced by MDA-MB-231 TNBC cells. Its expression is heavily downregulated in this cell line, as is the NAD+-dependent lysine deacetylase sirtuin 1 (SIRT1). I then showed that insulin-like growth factor 2 messenger RNA binding protein 2 (IGF2BP2), is a substrate of SIRT1, and its increased acetylation under conditions of low SIRT1 expression decreases the stability of the RNA transcript encoding TINAGL1. The exosomes from MDA-MB-231 cells stimulated AKT activity in recipient cancer cells and strongly promoted their ability to cell migrate and invade, which could be blocked by ectopically expressing TINAGL1 in the exosomes. Collectively, these results demonstrate that TNBC cell-derived EVs play essential roles within the TME to promote cancer progression.