Interleukin-1β modulates adhesion molecule expression and monocyte adhesion in glioblastoma

• Main Authors: Ching-Kai Shen, 沈靖凱
• Other Authors: Dah-Yuu Lu
• Format: Others
• Language: zh-TW
• Published: 2018
• Online Access: http://ndltd.ncl.edu.tw/handle/t5m74e

碩士 === 中國醫藥大學 === 生物醫學研究所碩士班 === 106 === Glioblastoma (GBM) is the most lethal brain tumor with highly inflammation in nature, infiltrated by microglia and surrounded by various pro-inflammatory cytokines. Cytokines are abundant in tumor microenvironment and involved in tumor progression. Adhesion molecules are known to mediate cell-cell interactions, particularly between immune cells and target tissues. ICAM-1 (also known as CD54) and VCAM-1 (also known as CD106) have been recognized as the major adhesion molecules of brain endothelial cells that facilitate attachment and penetration of leukocytes in the brain. However, the role of cytokines and adhesion molecules in monocyte/macrophage adhesion to human GBM is mostly unknown. In this study, we found that interleukin (IL)-1β induced ICAM-1 and VCAM-1 protein expression in a dose-dependent and time-dependent manner. In addition, IL-1β also induced ICAM-1 and VCAM-1 mRNA expression in a dose-dependent and time-dependent manner. Moreover, we also determined whether IL-1β induces ICAM and VCAM-1 expression and promotes human monocyte adhesion to GBM. The ability of monocytes to bind to GBM was determined using the monocyte-binding assay. Treatment of GBM with IL-1β increased THP-1 monocyte adhesion in a dose-dependent manner. Transfection with siRNA against ICAM-1 or VCAM-1 significantly decreased the expression of ICAM-1 and VCAM-1, and abolished the IL-1β-enhanced monocyte adhesion to GBM. Taken together, these results indicated that IL-1β-induced ICAM-1 and VCAM-1 expression are importantly modulators of adhesion of monocytes with GBM.