The role of mTORCs signaling in endothelial cell migration.
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 c...
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| Format: | Final Year Project (FYP) |
| Language: | English |
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2013
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| Online Access: | http://hdl.handle.net/10356/53794 |
| _version_ | 1826120996813275136 |
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| author | Liu, Shiyang. |
| author2 | Koh Cheng Gee |
| author_facet | Koh Cheng Gee Liu, Shiyang. |
| author_sort | Liu, Shiyang. |
| collection | NTU |
| description | 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. |
| first_indexed | 2024-10-01T05:25:33Z |
| format | Final Year Project (FYP) |
| id | ntu-10356/53794 |
| institution | Nanyang Technological University |
| language | English |
| last_indexed | 2024-10-01T05:25:33Z |
| publishDate | 2013 |
| record_format | dspace |
| spelling | ntu-10356/537942023-02-28T18:02:17Z The role of mTORCs signaling in endothelial cell migration. Liu, Shiyang. Koh Cheng Gee School of Biological Sciences DRNTU::Science::Biological sciences::Molecular biology 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. Bachelor of Science in Biological Sciences 2013-06-07T06:35:35Z 2013-06-07T06:35:35Z 2013 2013 Final Year Project (FYP) http://hdl.handle.net/10356/53794 en Nanyang Technological University 31 p. application/pdf |
| spellingShingle | DRNTU::Science::Biological sciences::Molecular biology Liu, Shiyang. The role of mTORCs signaling in endothelial cell migration. |
| title | The role of mTORCs signaling in endothelial cell migration. |
| title_full | The role of mTORCs signaling in endothelial cell migration. |
| title_fullStr | The role of mTORCs signaling in endothelial cell migration. |
| title_full_unstemmed | The role of mTORCs signaling in endothelial cell migration. |
| title_short | The role of mTORCs signaling in endothelial cell migration. |
| title_sort | role of mtorcs signaling in endothelial cell migration |
| topic | DRNTU::Science::Biological sciences::Molecular biology |
| url | http://hdl.handle.net/10356/53794 |
| work_keys_str_mv | AT liushiyang theroleofmtorcssignalinginendothelialcellmigration AT liushiyang roleofmtorcssignalinginendothelialcellmigration |