Exosome EpCAM promotes the metastasis of glioma by targeting the CD44 signaling molecule on the surface of glioma cells

Background.Glioma, the most common primary tumor in the central nervous system, originates from glial cells and has a poor prognosis.Objectives.This experimental laboratory study was designed to explore the role of epithelial cell adhesion molecule (EpCAM) in the metastasis of glioma.Material and methods.Serum samples were collected from patients with non-metastatic or metastatic glioma (n = 20 per group), and healthy volunteers (n = 8).Exosomes were isolated from the serum and the morphological characteristics were observed under a scanning electron microscope (SEM).The expression of CD81 and CD63 was measured to identify exosomes.Glioma tissue and the adjacent normal tissue samples were obtained from patients with non-metastatic or metastatic glioma (n = 12 per group).Meanwhile, 4 normal brain tissue samples were collected.The expression of CD44, hyaluronan-mediated motility receptor (HMMR), and matrix metalloproteinase-9 (MMP-9) was determined in each group using immunohistochemistry.The protein expression of CD44, HMMR, matrix metalloproteinase-2 (MMP-2), MMP-9, and selectin E (SELE) was measured with western blotting.Results.Exosomes were present in the serum, and the proteins CD81 and CD63 were expressed in all 3 groups.CD44 was highly expressed in the non-metastasis and metastasis groups.The expression of HMMR and MMP-9 in the Adj-metastasis and Adj-non-metastasis groups was high, while in the other groups, the levels were low.The expression of CD44 in the metastasis and non-metastasis groups was significantly higher than that of the negative control (NC) group, and the expression in the metastasis group was higher than that of the non-metastasis group.The MMP-2 and MMP-9 were not found in either the metastasis or non-metastasis group.The protein expression of HMMR and SELE was high in all groups.Conclusions.Exosome EpCAM promoted the metastasis of glioma by targeting CD44.