Abstract
Globally, gastric cancer (GC) ranks fourth in the incidence of malignant tumors. The early clinical manifestations of GC lack specificity. Most patients are already at an advanced stage when they are first diagnosed, and their late progression is mainly due to peritoneal metastasis. A pre-metastatic microenvironment is formed, before the macroscopic tumor metastasis. Extracellular vesicles (EVs) are nanovesicles released by cells into body fluids. Recent studies have shown that EVs can affect the tumor microenvironment by carrying cargos to participate in cell-to-cell communication. EVs derived from GC cells mediate the regulation of the pre-metastasis niche and act as a coordinator between tumor cells and normal stroma, immune cells, inflammatory cells, and tumor fibroblasts to promote tumor growth and metastasis. This review highlights the regulatory role of EVs in the pre-metastatic niche of GC and mulls EVs as a potential biomarker for liquid biopsy.
Highlights
Gastric cancer (GC) is one of the major global health problems
We summarized the roles of gastric cancer (GC)-derived Extracellular vesicles (EVs) in reshaping the pre-metastasis niche of GC which promotes the colonization and
Previous studies have shown that Cancer-associated fibroblasts (CAF) increased GC cell mobility and invasiveness by up-regulating Rhomboid 5 Homolog 2 (RHBDF2) expression through the Transforming growth factor b1 (TGF-b1) signaling pathway [76]
Summary
Gastric cancer (GC) is one of the major global health problems. There are about one million new cases of GC reported all over the world yearly [1, 2]. Extracellular vesicles; EGFR, Epidermal growth factor receptor; FZD10, Frizzled10; GC, Gastric cancer; HGF, Hepatocyte growth factor; TAMs, Tumor-associated macrophages; Treg, Regulatory T; TGF-b1, Transforming growth factor b1; Wnt, Wingless/Integrated; MAPK, Mitogen-activated protein kinase; MET, Mesenchymal-epithelial transition factor NA, Not available. In vitro experiments showed that GC-derived exosomes can be absorbed by peritoneal mesothelial cells and further up-regulate the expression of miR21-5p and directly target SMAD7 to promote peritoneal metastasis.
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