PI3K/AKT/mTOR signaling in gastric cancer: epigenetics and beyond.

Sadegh Fattahi; Fatemeh Amjadi-Moheb; Reza Tabaripour; Gholam Hossein Ashrafi; Haleh Akhavan-Niaki

doi:10.1016/j.lfs.2020.118513

PI3K/AKT/mTOR signaling in gastric cancer: epigenetics and beyond.

Sadegh Fattahi, Fatemeh Amjadi-Moheb, Reza Tabaripour, Gholam Hossein Ashrafi, Haleh Akhavan-Niaki

Research output: Contribution to journal › Article › peer-review

Abstract

PI3K/AKT/mTOR pathway is one of the most important signaling pathways involved in normal cellular processes. Its aberrant activation modulates autophagy, epithelial-mesenchymal transition, apoptosis, chemoresistance, and metastasis in many human cancers. Emerging evidence demonstrates that some infections as well as epigenetic regulatory mechanisms can control PI3K/AKT/mTOR signaling pathway. In this review, we focused on the role of this pathway in gastric cancer development, prognosis, and metastasis, with an emphasis on epigenetic alterations including DNA methylation, histone modifications, and post-transcriptional modulations through non-coding RNAs fluctuations as well as H. pylori and Epstein-Barr virus infections. Finally, we reviewed different molecular targets and therapeutic agents in clinical trials as a potential strategy for gastric cancer treatment through the PI3K/AKT/mTOR pathway. [Abstract copyright: Copyright © 2020 Elsevier Inc. All rights reserved.]

Original language	English
Article number	118513
Journal	Life Sciences
Volume	262
Early online date	1 Oct 2020
DOIs	https://doi.org/10.1016/j.lfs.2020.118513
Publication status	Published - 1 Dec 2020

Keywords

Chemoresistance
Epigenetic modulation
Gastric cancer
Non-coding RNAs
PI3K/AKT/mTOR pathway
Pre-clinical and human biological sciences
Targeted therapy

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10.1016/j.lfs.2020.118513

Ashrafi-H-47265-AAMAccepted author manuscript, 698 KBLicence: CC BY-NC-ND

https://doi.org/10.1016/j.lfs.2020.118513

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title = "PI3K/AKT/mTOR signaling in gastric cancer: epigenetics and beyond.",

abstract = "PI3K/AKT/mTOR pathway is one of the most important signaling pathways involved in normal cellular processes. Its aberrant activation modulates autophagy, epithelial-mesenchymal transition, apoptosis, chemoresistance, and metastasis in many human cancers. Emerging evidence demonstrates that some infections as well as epigenetic regulatory mechanisms can control PI3K/AKT/mTOR signaling pathway. In this review, we focused on the role of this pathway in gastric cancer development, prognosis, and metastasis, with an emphasis on epigenetic alterations including DNA methylation, histone modifications, and post-transcriptional modulations through non-coding RNAs fluctuations as well as H. pylori and Epstein-Barr virus infections. Finally, we reviewed different molecular targets and therapeutic agents in clinical trials as a potential strategy for gastric cancer treatment through the PI3K/AKT/mTOR pathway. [Abstract copyright: Copyright {\textcopyright} 2020 Elsevier Inc. All rights reserved.]",

keywords = "Chemoresistance, Epigenetic modulation, Gastric cancer, Non-coding RNAs, PI3K/AKT/mTOR pathway, Pre-clinical and human biological sciences, Targeted therapy",

author = "Sadegh Fattahi and Fatemeh Amjadi-Moheb and Reza Tabaripour and Ashrafi, \{Gholam Hossein\} and Haleh Akhavan-Niaki",

year = "2020",

month = dec,

day = "1",

doi = "10.1016/j.lfs.2020.118513",

language = "English",

volume = "262",

journal = "Life Sciences",

issn = "0024-3205",

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TY - JOUR

T1 - PI3K/AKT/mTOR signaling in gastric cancer

T2 - epigenetics and beyond.

AU - Fattahi, Sadegh

AU - Amjadi-Moheb, Fatemeh

AU - Tabaripour, Reza

AU - Ashrafi, Gholam Hossein

AU - Akhavan-Niaki, Haleh

PY - 2020/12/1

Y1 - 2020/12/1

N2 - PI3K/AKT/mTOR pathway is one of the most important signaling pathways involved in normal cellular processes. Its aberrant activation modulates autophagy, epithelial-mesenchymal transition, apoptosis, chemoresistance, and metastasis in many human cancers. Emerging evidence demonstrates that some infections as well as epigenetic regulatory mechanisms can control PI3K/AKT/mTOR signaling pathway. In this review, we focused on the role of this pathway in gastric cancer development, prognosis, and metastasis, with an emphasis on epigenetic alterations including DNA methylation, histone modifications, and post-transcriptional modulations through non-coding RNAs fluctuations as well as H. pylori and Epstein-Barr virus infections. Finally, we reviewed different molecular targets and therapeutic agents in clinical trials as a potential strategy for gastric cancer treatment through the PI3K/AKT/mTOR pathway. [Abstract copyright: Copyright © 2020 Elsevier Inc. All rights reserved.]

AB - PI3K/AKT/mTOR pathway is one of the most important signaling pathways involved in normal cellular processes. Its aberrant activation modulates autophagy, epithelial-mesenchymal transition, apoptosis, chemoresistance, and metastasis in many human cancers. Emerging evidence demonstrates that some infections as well as epigenetic regulatory mechanisms can control PI3K/AKT/mTOR signaling pathway. In this review, we focused on the role of this pathway in gastric cancer development, prognosis, and metastasis, with an emphasis on epigenetic alterations including DNA methylation, histone modifications, and post-transcriptional modulations through non-coding RNAs fluctuations as well as H. pylori and Epstein-Barr virus infections. Finally, we reviewed different molecular targets and therapeutic agents in clinical trials as a potential strategy for gastric cancer treatment through the PI3K/AKT/mTOR pathway. [Abstract copyright: Copyright © 2020 Elsevier Inc. All rights reserved.]

KW - Chemoresistance

KW - Epigenetic modulation

KW - Gastric cancer

KW - Non-coding RNAs

KW - PI3K/AKT/mTOR pathway

KW - Pre-clinical and human biological sciences

KW - Targeted therapy

U2 - 10.1016/j.lfs.2020.118513

DO - 10.1016/j.lfs.2020.118513

M3 - Article

SN - 0024-3205

VL - 262

JO - Life Sciences

JF - Life Sciences

M1 - 118513

ER -

PI3K/AKT/mTOR signaling in gastric cancer: epigenetics and beyond.

Abstract

Keywords

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