Exploiting cancer vulnerabilities: mTOR, autophagy, and homeostatic imbalance

Johnson, Charlotte E. ORCID: https://orcid.org/0000-0003-1954-5142 and Tee, Andrew R. ORCID: https://orcid.org/0000-0002-5577-4631 2017. Exploiting cancer vulnerabilities: mTOR, autophagy, and homeostatic imbalance. Essays in Biochemistry 61 (6) , pp. 699-710. 10.1042/EBC20170056

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Abstract

Mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) at lysosomes plays a pivotal role in cell growth control where an array of large multiprotein complexes relay nutrient, energy, and growth signal inputs through mTORC1. In cancer cells, such regulation often becomes disconnected, leading to uncontrolled cell growth and an elevation in cellular stress. Consequently, cancer cells often lose homeostatic balance as they grow in unfavorable conditions, i.e. when nutrients and energy are limited yet mTORC1 is still aberrantly activated. Cancer cells lose signaling flexibility because of hyperactive mTORC1 that leads to heightened cellular stress and loss of nutrient and energy homeostasis, all of which are potential avenues for cancer therapy. Cancer cells often enhance mTORC1 to drive cell growth and proliferation, while also maintaining their survival. Autophagy regulation by mTORC1 is critically involved in nutrient and energy homeostasis, cell growth control, and survival. Studying mTORC1 and autophagy as a potential therapeutic target for cancer treatment has been the focus of a wide range of research over the past few decades. This review will explore the signaling pathways central to mTORC1 and autophagy regulation, and cancer vulnerabilities while considering anticancer therapies.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Publisher:	Portland Press
ISSN:	0071-1365
Date of First Compliant Deposit:	5 February 2018
Date of Acceptance:	12 December 2017
Last Modified:	29 Nov 2024 06:00
URI:	https://orca.cardiff.ac.uk/id/eprint/108849

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