Abstract

Abstract Cell migration is central for many physiological and pathological processes, including embryogenesis, tissue repair, inflammatory responses, and cancer metastasis. Focal adhesion (FA) turnover has been demonstrated to play important role in controlling cell migration. Recently, FA disassembly was shown to be regulated by endocytosis during cell migration. Rabs are GTPase proteins that participate in various cellular vesicle transports; however, whether Rab proteins play the role in mediating vesicle transport for FA formation is not clear. This study is examining whether Rab11 mediated endosome recycling regulates FA formation during cell migration. Rab11 Wild-type, dominant negative or shRNA were transfected into human HT1080 fibrosarcoma cells, the cell motility was determined by trans-well assay and random migration assay, the localization of Rab11 and focal adhesion molecules were monitored by confocal microscopy. Results showed the Rab11 dominant negative form or shRNA transfection inhibited chemoattractive cell migration, however, only the Rab11 shRNA transfection inhibited random cell migration. Rab11 was also found colocalized with recycled β1 integrin and focal adhesion kinase and affected focal adhesion formation. Taken together, the results suggested Rab11 affected cell migration by regulating FAK dynamics and the activity of Rab11 is required for external stimulation. The interaction of Rab11 with associated focal adhesion molecules will be further investigated. Citation Format: Ling-Yi Kao, Yi-Che Wu, Wei-Ting Chao. Rab11 mediated focal adhesion turnover in sarcoma cell migration. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-69. doi:10.1158/1538-7445.AM2014-LB-69

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