Deregulation of the akt pathway in human cancer

Eriko Tokunaga, Eiji Oki, Akinori Egashira, Noriaki Sadanaga, Masaru Morita, Yoshihiro Kakeji, Yoshihiko Maehara

Research output: Contribution to journalReview article

175 Citations (Scopus)

Abstract

Akt (protein kinase B) is a serine/threonine kinase which is a central regulator of widely divergent cellular processes including proliferation, differentiation, migration, survival and metabolism. Akt is activated by a variety of stimuli, through growth factor receptors, in phosphatidylinositol 3-kinase (PI3K)-dependent manner. Akt is also negatively regulated by the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN). A disruption of normal Akt/PKB/PTEN signaling frequently occurs in many human cancers, which plays an important role in cancer development, progression and therapeutic resistance. Numerous studies have revealed the blockage of Akt signaling to result in apoptosis and growth inhibition of tumor cells. Therefore, this signaling pathway, including both upstream and downstream of Akt, has recently attracted considerable attention as a new target for effective cancer therapeutic strategies. In fact, many inhibitors of Akt pathway have been identified and clinical studies of some agents are ongoing. In this review, we describe Akt signaling pathway components and its cellular functions as well as the alterations in human cancers and the therapeutic approaches for targeting the Akt pathway in cancer.

Original languageEnglish
Pages (from-to)27-36
Number of pages10
JournalCurrent Cancer Drug Targets
Volume8
Issue number1
DOIs
Publication statusPublished - Feb 1 2008

Fingerprint

Neoplasms
Phosphatidylinositol 3-Kinase
Chromosomes, Human, Pair 10
Proto-Oncogene Proteins c-akt
Growth Factor Receptors
Protein-Serine-Threonine Kinases
Phosphoric Monoester Hydrolases
Therapeutics
Apoptosis
Survival
Growth

All Science Journal Classification (ASJC) codes

  • Oncology
  • Pharmacology
  • Drug Discovery
  • Cancer Research

Cite this

Tokunaga, E., Oki, E., Egashira, A., Sadanaga, N., Morita, M., Kakeji, Y., & Maehara, Y. (2008). Deregulation of the akt pathway in human cancer. Current Cancer Drug Targets, 8(1), 27-36. https://doi.org/10.2174/156800908783497140

Deregulation of the akt pathway in human cancer. / Tokunaga, Eriko; Oki, Eiji; Egashira, Akinori; Sadanaga, Noriaki; Morita, Masaru; Kakeji, Yoshihiro; Maehara, Yoshihiko.

In: Current Cancer Drug Targets, Vol. 8, No. 1, 01.02.2008, p. 27-36.

Research output: Contribution to journalReview article

Tokunaga, E, Oki, E, Egashira, A, Sadanaga, N, Morita, M, Kakeji, Y & Maehara, Y 2008, 'Deregulation of the akt pathway in human cancer', Current Cancer Drug Targets, vol. 8, no. 1, pp. 27-36. https://doi.org/10.2174/156800908783497140
Tokunaga E, Oki E, Egashira A, Sadanaga N, Morita M, Kakeji Y et al. Deregulation of the akt pathway in human cancer. Current Cancer Drug Targets. 2008 Feb 1;8(1):27-36. https://doi.org/10.2174/156800908783497140
Tokunaga, Eriko ; Oki, Eiji ; Egashira, Akinori ; Sadanaga, Noriaki ; Morita, Masaru ; Kakeji, Yoshihiro ; Maehara, Yoshihiko. / Deregulation of the akt pathway in human cancer. In: Current Cancer Drug Targets. 2008 ; Vol. 8, No. 1. pp. 27-36.
@article{45c733b6fb1341cab8c2435c369cfb4c,
title = "Deregulation of the akt pathway in human cancer",
abstract = "Akt (protein kinase B) is a serine/threonine kinase which is a central regulator of widely divergent cellular processes including proliferation, differentiation, migration, survival and metabolism. Akt is activated by a variety of stimuli, through growth factor receptors, in phosphatidylinositol 3-kinase (PI3K)-dependent manner. Akt is also negatively regulated by the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN). A disruption of normal Akt/PKB/PTEN signaling frequently occurs in many human cancers, which plays an important role in cancer development, progression and therapeutic resistance. Numerous studies have revealed the blockage of Akt signaling to result in apoptosis and growth inhibition of tumor cells. Therefore, this signaling pathway, including both upstream and downstream of Akt, has recently attracted considerable attention as a new target for effective cancer therapeutic strategies. In fact, many inhibitors of Akt pathway have been identified and clinical studies of some agents are ongoing. In this review, we describe Akt signaling pathway components and its cellular functions as well as the alterations in human cancers and the therapeutic approaches for targeting the Akt pathway in cancer.",
author = "Eriko Tokunaga and Eiji Oki and Akinori Egashira and Noriaki Sadanaga and Masaru Morita and Yoshihiro Kakeji and Yoshihiko Maehara",
year = "2008",
month = "2",
day = "1",
doi = "10.2174/156800908783497140",
language = "English",
volume = "8",
pages = "27--36",
journal = "Current Cancer Drug Targets",
issn = "1568-0096",
publisher = "Bentham Science Publishers B.V.",
number = "1",

}

TY - JOUR

T1 - Deregulation of the akt pathway in human cancer

AU - Tokunaga, Eriko

AU - Oki, Eiji

AU - Egashira, Akinori

AU - Sadanaga, Noriaki

AU - Morita, Masaru

AU - Kakeji, Yoshihiro

AU - Maehara, Yoshihiko

PY - 2008/2/1

Y1 - 2008/2/1

N2 - Akt (protein kinase B) is a serine/threonine kinase which is a central regulator of widely divergent cellular processes including proliferation, differentiation, migration, survival and metabolism. Akt is activated by a variety of stimuli, through growth factor receptors, in phosphatidylinositol 3-kinase (PI3K)-dependent manner. Akt is also negatively regulated by the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN). A disruption of normal Akt/PKB/PTEN signaling frequently occurs in many human cancers, which plays an important role in cancer development, progression and therapeutic resistance. Numerous studies have revealed the blockage of Akt signaling to result in apoptosis and growth inhibition of tumor cells. Therefore, this signaling pathway, including both upstream and downstream of Akt, has recently attracted considerable attention as a new target for effective cancer therapeutic strategies. In fact, many inhibitors of Akt pathway have been identified and clinical studies of some agents are ongoing. In this review, we describe Akt signaling pathway components and its cellular functions as well as the alterations in human cancers and the therapeutic approaches for targeting the Akt pathway in cancer.

AB - Akt (protein kinase B) is a serine/threonine kinase which is a central regulator of widely divergent cellular processes including proliferation, differentiation, migration, survival and metabolism. Akt is activated by a variety of stimuli, through growth factor receptors, in phosphatidylinositol 3-kinase (PI3K)-dependent manner. Akt is also negatively regulated by the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN). A disruption of normal Akt/PKB/PTEN signaling frequently occurs in many human cancers, which plays an important role in cancer development, progression and therapeutic resistance. Numerous studies have revealed the blockage of Akt signaling to result in apoptosis and growth inhibition of tumor cells. Therefore, this signaling pathway, including both upstream and downstream of Akt, has recently attracted considerable attention as a new target for effective cancer therapeutic strategies. In fact, many inhibitors of Akt pathway have been identified and clinical studies of some agents are ongoing. In this review, we describe Akt signaling pathway components and its cellular functions as well as the alterations in human cancers and the therapeutic approaches for targeting the Akt pathway in cancer.

UR - http://www.scopus.com/inward/record.url?scp=39049151617&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=39049151617&partnerID=8YFLogxK

U2 - 10.2174/156800908783497140

DO - 10.2174/156800908783497140

M3 - Review article

C2 - 18288941

AN - SCOPUS:39049151617

VL - 8

SP - 27

EP - 36

JO - Current Cancer Drug Targets

JF - Current Cancer Drug Targets

SN - 1568-0096

IS - 1

ER -