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mTOR Signaling Components in Tumor Mechanobiology

Mechanistic target of rapamycin (mTOR) is a central signaling hub that integrates networks of nutrient availability, cellular metabolism, and autophagy in eukaryotic cells. mTOR kinase, along with its upstream regulators and downstream substrates, is upregulated in most human malignancies. At the sa...

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Autores principales: Gargalionis, Antonios N., Papavassiliou, Kostas A., Basdra, Efthimia K., Papavassiliou, Athanasios G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8837098/
https://www.ncbi.nlm.nih.gov/pubmed/35163745
http://dx.doi.org/10.3390/ijms23031825
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author Gargalionis, Antonios N.
Papavassiliou, Kostas A.
Basdra, Efthimia K.
Papavassiliou, Athanasios G.
author_facet Gargalionis, Antonios N.
Papavassiliou, Kostas A.
Basdra, Efthimia K.
Papavassiliou, Athanasios G.
author_sort Gargalionis, Antonios N.
collection PubMed
description Mechanistic target of rapamycin (mTOR) is a central signaling hub that integrates networks of nutrient availability, cellular metabolism, and autophagy in eukaryotic cells. mTOR kinase, along with its upstream regulators and downstream substrates, is upregulated in most human malignancies. At the same time, mechanical forces from the tumor microenvironment and mechanotransduction promote cancer cells’ proliferation, motility, and invasion. mTOR signaling pathway has been recently found on the crossroads of mechanoresponsive-induced signaling cascades to regulate cell growth, invasion, and metastasis in cancer cells. In this review, we examine the emerging association of mTOR signaling components with certain protein tools of tumor mechanobiology. Thereby, we highlight novel mechanisms of mechanotransduction, which regulate tumor progression and invasion, as well as mechanisms related to the therapeutic efficacy of antitumor drugs.
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spelling pubmed-88370982022-02-12 mTOR Signaling Components in Tumor Mechanobiology Gargalionis, Antonios N. Papavassiliou, Kostas A. Basdra, Efthimia K. Papavassiliou, Athanasios G. Int J Mol Sci Review Mechanistic target of rapamycin (mTOR) is a central signaling hub that integrates networks of nutrient availability, cellular metabolism, and autophagy in eukaryotic cells. mTOR kinase, along with its upstream regulators and downstream substrates, is upregulated in most human malignancies. At the same time, mechanical forces from the tumor microenvironment and mechanotransduction promote cancer cells’ proliferation, motility, and invasion. mTOR signaling pathway has been recently found on the crossroads of mechanoresponsive-induced signaling cascades to regulate cell growth, invasion, and metastasis in cancer cells. In this review, we examine the emerging association of mTOR signaling components with certain protein tools of tumor mechanobiology. Thereby, we highlight novel mechanisms of mechanotransduction, which regulate tumor progression and invasion, as well as mechanisms related to the therapeutic efficacy of antitumor drugs. MDPI 2022-02-05 /pmc/articles/PMC8837098/ /pubmed/35163745 http://dx.doi.org/10.3390/ijms23031825 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Gargalionis, Antonios N.
Papavassiliou, Kostas A.
Basdra, Efthimia K.
Papavassiliou, Athanasios G.
mTOR Signaling Components in Tumor Mechanobiology
title mTOR Signaling Components in Tumor Mechanobiology
title_full mTOR Signaling Components in Tumor Mechanobiology
title_fullStr mTOR Signaling Components in Tumor Mechanobiology
title_full_unstemmed mTOR Signaling Components in Tumor Mechanobiology
title_short mTOR Signaling Components in Tumor Mechanobiology
title_sort mtor signaling components in tumor mechanobiology
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8837098/
https://www.ncbi.nlm.nih.gov/pubmed/35163745
http://dx.doi.org/10.3390/ijms23031825
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