| Summary: | 碩士 === 國立臺灣大學 === 生化科技學系 === 102 === Cancer is caused by abnormal growth or division of cell and it can mainly be divided into two types: benign neoplasms and malignant neoplasms. The characteristics of malignant neoplasms are tumor cells with metastatic ability. It has been shown that matrix metalloproteinases 9 (MMP9) plays an important role in tumor progression and metastasis. MMP9 can help the digestion of extracellular matrix and is an important marker of invasion and metastasis. Chloride intracellular channel 4 (CLIC4) is a chloride intracellular channel protein, which involved in many cellular functions like apoptosis, angiogenesis, tumor progression and invasion. Previously, we have found that CLIC4 will affect the invasion ability through the regulation of MMP9 expression. The purpose of this study is to investigate how CLIC4 regulate MMP9 expression. We first use CLIC4 siRNA to knockdown the expression level of CLIC4 in MDA-MB 231 cells. The mRNA expression level and the activity of MMP9 decrease when the expression level of CLIC4 was knockdowned. These results indicated that CLIC4 might play a role in regulating the MMP9 expression. Furthermore, luciferase reporter with different MMP9 promoter region was used to examine the possible transcriptional factor involved in CLIC4-mediated MMP9 expression. Finally, immunocomplex pull-downed by antibody against CLIC4 was analyzed by LC-MS/MS. Some candidates of possible transcriptional factors and signal transduction pathways have been found.
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