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|Title:||The role of mTORCs signaling in endothelial cell migration.||Authors:||Liu, Shiyang.||Keywords:||DRNTU::Science::Biological sciences::Molecular biology||Issue Date:||2013||Abstract:||The Mammalian target of rapamycin (mTOR) is a serine/ threonine kinase that functions as two distinct complexes, mTORC1 and mTORC2. Both of them have been shown to be involved in cell migration via different downstream effectors, among which Rho-family small GTPases play crucial roles. Endothelial cell migration is an integral part of angiogenesis, which is a vital process in various physiological and pathological conditions. However, few studies have been done to investigate the role of mTORCs signaling in endothelial cell migration and whether Rho-family small GTPases are involved in this process. In this study, we demonstrated that knockdown of raptor, a core component of mTORC1, reduced the migration of HUVECs, the lamellipodia formation and its Rac1 activity. However, knockdown of rictor, a core component of mTORC2, appeared to exert opposite effects on HUVECs motility: in wound healing assay, rictor depletion reduced the spontaneous motility of HUVECs; whereas, silencing rictor enhanced both spontaneous and induced HUVECs motility in transwell migration assay. Upregulated Rac1 activity and disrupted lamellipodia formation were also observed in rictor-knockdown HUVECs. In addition, a compensatory relationship between rictor and raptor in HUVECs was identified, which might further complicate the role of mTORCs signaling in endothelial cell migration.||URI:||http://hdl.handle.net/10356/53794||Rights:||Nanyang Technological University||Fulltext Permission:||restricted||Fulltext Availability:||With Fulltext|
|Appears in Collections:||SBS Student Reports (FYP/IA/PA/PI)|
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