| Summary: | 碩士 === 長庚大學 === 生物醫學研究所 === 100 === Mac-2 binding protein (Mac-2 BP) is a secreted glycoprotein of 90-100 kDa. Although elevated Mac-2 BP levels have been observed in tissues and sera of patients with various cancer types, the functions of Mac-2 BP remain largely unknown. Previous study from our lab revealed that Mac-2 BP is overexpressed in oral squamous cell carcinoma (OSCC) and could be highly secreted by OSCC cell lines. Furthermore, Mac-2 BP knockdown in OEC-M1 caused drastic inhibition of cell migration, suggesting that Mac-2 BP may play an important role in the mobility of OSCC cells. In this study, we investigate the global effect of Mac-2 BP knockdown in OC3 cells on the total cell proteome and the secreted proteome (secretome). Since previously researches have reported that ECM-integrin signaling pathway may improve cell mobility, these data imply that Mac-2 BP may participate in ECM-integrin signaling pathway, and stably knocked down Mac-2 BP alters cell mobility by regulating cell adhesion or blocking the signal transduction. Quantifying confocal microscope image of immunofluorescence staining indicated that the average size but not the number of focal adhesions was larger in Mac-2 BP knockdown (KD) cells than in control cells. However, we could not observe the difference in cell adhesion function. Moreover, FAK activation of Mac-2 BP knock down cells showed low sensitivity to FN stimulation, although the phenomenon is not significant. These results demonstrate that Mac-2 BP may affect multiple pathways, and the slightly change of adhesive ability is not the main factor for altering cell mobility. Additionally, the bioinformatics analysis show the dramatic change of secretome in Mac-2 BP KD cells, which may be caused by exceptional transportation and secretion. These results indicate that Mac-2 BP may in turn affect cell mobility by varying the signal equilibrium.
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