Med28 (Magicin) Regulates Migration and Cell Cycle Progression in MCF-7 Human Breast Cancer Cells

• Main Authors: Yu-Hsuan Chou, 周毓軒
• Other Authors: Chun-Yin Huang
• Format: Others
• Language: zh-TW
• Published: 2011
• Online Access: http://ndltd.ncl.edu.tw/handle/37915155680884843493

碩士 === 中國醫藥大學 === 營養學系碩士班 === 99 === Magicin (Med28) exhibits multiple cellular roles. The interaction of Med28 with Grb2, Src, merlin, and actin cytoskeleton, strongly suggests that Med28 involves in many cellular signaling pathways. Several tumors overexpress Med28, whereas the role of Med28 in tumor development is unclear. The objective of this study is to understand the role of Med28 in cellular migration and proliferation using Med28 over-expressing MCF-7 breast cancer cells as a model. RNA interference-mediated depletion of Med28 inhibited cellular migration and matrix metalloproteinase-2 (MMP-2) activation in MCF-7 cells. In addition, Med28 siRNA delayed cell cycle progression, decreased cyclin D1 expression, and increased HMG-box transcription factor 1 (HBP1) expression. The disruption of Med28 also inhibited the expression of several migration-related signaling molecules, including MEK1. In Med28-overexpressing cells, RNA interference-mediated depletion of MEK-1 inhibited migration with a respectively decreasing matrix metalloproteinase-2 (MMP-2) activation. These data suggest that Med28 might regulate MMP-2-mediated cellular migration via MEK1/ERK signaling pathway. Taken together, our data demonstrate that Med28 involves in cellular migration and proliferation in breast cancer cells, which may have clinical application in the intervention of breast cancer.