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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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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
Online Access: Check full text

URI: https://cronfa.swan.ac.uk/Record/cronfa58770
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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 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.
Keywords: mTOR; cancer; cell growth; S6K1; 4E-BP1; eIF4E; HIF; STAT3; SGK1
College: Swansea University Medical School
Funders: 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).
Issue: 1
Start Page: 5