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Oncogenic Signalling through Mechanistic Target of Rapamycin (mTOR): A Driver of Metabolic Transformation and Cancer Progression

Ellie Rad, James Murray Orcid Logo, Andrew Tee

Cancers, Volume: 10, Issue: 1, Start page: 5

Swansea University Author: James Murray Orcid Logo

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DOI (Published version): 10.3390/cancers10010005

Abstract

Throughout the years, research into signalling pathways involved in cancer progression has led to many discoveries of which mechanistic target of rapamycin (mTOR) is a key player. mTOR is a master regulator of cell growth control. mTOR is historically known to promote cell growth by enhancing the ef...

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Published in: Cancers
ISSN: 2072-6694
Published: MDPI AG 2018
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URI: https://cronfa.swan.ac.uk/Record/cronfa58770
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first_indexed 2021-12-03T15:28:27Z
last_indexed 2021-12-04T04:17:58Z
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spelling 2021-12-03T15:31:17.3541046 v2 58770 2021-11-24 Oncogenic Signalling through Mechanistic Target of Rapamycin (mTOR): A Driver of Metabolic Transformation and Cancer Progression 12d0a585fcfe66f83c4c21c6bca3197b 0000-0002-6928-2347 James Murray James Murray true false 2021-11-24 BMS Throughout the years, research into signalling pathways involved in cancer progression has led to many discoveries of which mechanistic target of rapamycin (mTOR) is a key player. mTOR is a master regulator of cell growth control. mTOR is historically known to promote cell growth by enhancing the efficiency of protein translation. Research in the last decade has revealed that mTOR’s role in promoting cell growth is much more multifaceted. While mTOR is necessary for normal human physiology, cancer cells take advantage of mTOR signalling to drive their neoplastic growth and progression. Oncogenic signal transduction through mTOR is a common occurrence in cancer, leading to metabolic transformation, enhanced proliferative drive and increased metastatic potential through neovascularisation. This review focuses on the downstream mTOR-regulated processes that are implicated in the “hallmarks” of cancer with focus on mTOR’s involvement in proliferative signalling, metabolic reprogramming, angiogenesis and metastasis. Journal Article Cancers 10 1 5 MDPI AG 2072-6694 mTOR; cancer; cell growth; S6K1; 4E-BP1; eIF4E; HIF; STAT3; SGK1 3 1 2018 2018-01-03 10.3390/cancers10010005 COLLEGE NANME Biomedical Sciences COLLEGE CODE BMS Swansea University Cancer Research Wales (grant number 508502 (to Andrew R. Tee)); the Health and Care Research Wales (the Wales Cancer Research Centre) (grant number CA05); the Tuberous Sclerosis Association and the Tuberous Sclerosis Alliance (grant number 2013-P05, and 03-15). 2021-12-03T15:31:17.3541046 2021-11-24T13:54:12.4028690 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine Ellie Rad 1 James Murray 0000-0002-6928-2347 2 Andrew Tee 3 58770__21781__7b7aef758a4e4a85b6acd01dc36cf0bc.pdf 58770.pdf 2021-12-03T15:28:53.9427511 Output 1663310 application/pdf Version of Record true © 2018 by the authors. This is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license true eng http://creativecommons.org/licenses/by/4.0/
title Oncogenic Signalling through Mechanistic Target of Rapamycin (mTOR): A Driver of Metabolic Transformation and Cancer Progression
spellingShingle Oncogenic Signalling through Mechanistic Target of Rapamycin (mTOR): A Driver of Metabolic Transformation and Cancer Progression
James Murray
title_short Oncogenic Signalling through Mechanistic Target of Rapamycin (mTOR): A Driver of Metabolic Transformation and Cancer Progression
title_full Oncogenic Signalling through Mechanistic Target of Rapamycin (mTOR): A Driver of Metabolic Transformation and Cancer Progression
title_fullStr Oncogenic Signalling through Mechanistic Target of Rapamycin (mTOR): A Driver of Metabolic Transformation and Cancer Progression
title_full_unstemmed Oncogenic Signalling through Mechanistic Target of Rapamycin (mTOR): A Driver of Metabolic Transformation and Cancer Progression
title_sort Oncogenic Signalling through Mechanistic Target of Rapamycin (mTOR): A Driver of Metabolic Transformation and Cancer Progression
author_id_str_mv 12d0a585fcfe66f83c4c21c6bca3197b
author_id_fullname_str_mv 12d0a585fcfe66f83c4c21c6bca3197b_***_James Murray
author James Murray
author2 Ellie Rad
James Murray
Andrew Tee
format Journal article
container_title Cancers
container_volume 10
container_issue 1
container_start_page 5
publishDate 2018
institution Swansea University
issn 2072-6694
doi_str_mv 10.3390/cancers10010005
publisher MDPI AG
college_str Faculty of Medicine, Health and Life Sciences
hierarchytype
hierarchy_top_id facultyofmedicinehealthandlifesciences
hierarchy_top_title Faculty of Medicine, Health and Life Sciences
hierarchy_parent_id facultyofmedicinehealthandlifesciences
hierarchy_parent_title Faculty of Medicine, Health and Life Sciences
department_str Swansea University Medical School - Medicine{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Medicine
document_store_str 1
active_str 0
description Throughout the years, research into signalling pathways involved in cancer progression has led to many discoveries of which mechanistic target of rapamycin (mTOR) is a key player. mTOR is a master regulator of cell growth control. mTOR is historically known to promote cell growth by enhancing the efficiency of protein translation. Research in the last decade has revealed that mTOR’s role in promoting cell growth is much more multifaceted. While mTOR is necessary for normal human physiology, cancer cells take advantage of mTOR signalling to drive their neoplastic growth and progression. Oncogenic signal transduction through mTOR is a common occurrence in cancer, leading to metabolic transformation, enhanced proliferative drive and increased metastatic potential through neovascularisation. This review focuses on the downstream mTOR-regulated processes that are implicated in the “hallmarks” of cancer with focus on mTOR’s involvement in proliferative signalling, metabolic reprogramming, angiogenesis and metastasis.
published_date 2018-01-03T04:15:34Z
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score 11.013148

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