| Summary: | 碩士 === 長庚大學 === 生物醫學研究所 === 100 === ADP-ribosylation factors like protein 1 (ARL1) is a member of the ARF/ARL family of the Ras-like GTPase superfamily. ARL1 is enriched in the trans-Golgi network (TGN) and has been proposed involved in endocytosis and exocytosis. However, the physiological function of ARL1 remains to be deciphered. Herein, we applied the siRNA approach to knock down endogenous ARL1 and one of its effector, Golgin-97, respectively followed by examining the phenotypic changes in knockdown cell. By using immunofluorescence assay, we found that knockdown of ARL1 or Golgin-97 decreased the cell membrane distributed E-cadherin in MCF-7 cells. Migration and invasion assay showed that knockdown of ARL1 or Golgin-97 promoted cell migration and invasion. We also found that ARL1 and Golgin-97 regulated the secreted metalloproteinase (MMP-9 and MMP2) in conditioned media. In addition, the promoted invasion effects shown in Golgin-97 knockdown cell were rescued by overexpressed wild-type Golgin-97, but not ARL1 interaction-defected construct. Collectively, our results suggest that Golgin-97 play roles on cell migration/invasion and conclude that this regulation might be in a ARL1-dependent manner. The future investigations would aim for comparatively analyzing the differential protein profiles in conditioned media (secretome) of Golgin-97 knockdown cells by quantitative proteomic approaches to reveal the Golgin-97-mediated protein secretion and cell migration/invasion.
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