Exploiting cancer vulnerabilities: mTOR, autophagy, and homeostatic imbalance
Autor: | Charlotte E. Johnson, Andrew R. Tee |
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Jazyk: | angličtina |
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
mTORC1 Biology Biochemistry Energy homeostasis 03 medical and health sciences Neoplasms Autophagy medicine Animals Autophagy-Related Protein-1 Homolog Homeostasis Humans Molecular Biology Mechanistic target of rapamycin PI3K/AKT/mTOR pathway Cell growth TOR Serine-Threonine Kinases Cancer Endoplasmic Reticulum Stress medicine.disease Cell biology 030104 developmental biology Cancer cell biology.protein biological phenomena cell phenomena and immunity Signal Transduction |
ISSN: | 0071-1365 |
Popis: | 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. |
Databáze: | OpenAIRE |
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