Primers on molecular pathways: The glycogen synthase kinase-3β

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Despite tremendous scientific effort, conventional treatment approaches have had little impact on the course of pancreatic ductal adenocarcinoma. Therefore, urgency is needed to understand the molecular mechanisms underlying the development of pancreatic cancer with the hope that this will lead to preventative and treatment strategies to improve the outcome of the disease. Numerous factors contribute to progression of this disease, including constitutively active NFκB, which has been shown to positively influence cancer cell survival, proliferation, invasion, metastasis and chemoresistance. Recently, the cytoplasmic serine/threonine protein kinase glycogen synthase kinase-3β (GSK-3β) was found to regulate NFκB activation and the proliferation and survival of pancreatic cancer cells. Moreover, recent studies in other human malignancies have implicated GSK-3β as a regulator of cancer cell proliferation, survival and chemoresistance through distinct mechanisms. Thus, GSK-3β has emerged as a viable therapeutic target in the treatment of several human neoplasms.

Original languageEnglish (US)
Pages (from-to)398-402
Number of pages5
JournalPancreatology
Volume7
Issue number5-6
DOIs
StatePublished - Oct 2007

Fingerprint

Glycogen Synthase Kinase 3
Pancreatic Neoplasms
Neoplasms
Cell Survival
Cell Proliferation
Protein-Serine-Threonine Kinases
Disease Progression
Adenocarcinoma
Neoplasm Metastasis
Survival

Keywords

  • β-Catenin
  • Glycogen synthase
  • Glycogen synthase kinase-3
  • Heterochromatin
  • NFκB
  • Pancreatic adenocarcinoma

ASJC Scopus subject areas

  • Endocrinology
  • Gastroenterology

Cite this

Primers on molecular pathways : The glycogen synthase kinase-3β. / Billadeau, Daniel D.

In: Pancreatology, Vol. 7, No. 5-6, 10.2007, p. 398-402.

Research output: Contribution to journalArticle

@article{3b2a1fb7907b4dabbf115394eb7ef31c,
title = "Primers on molecular pathways: The glycogen synthase kinase-3β",
abstract = "Despite tremendous scientific effort, conventional treatment approaches have had little impact on the course of pancreatic ductal adenocarcinoma. Therefore, urgency is needed to understand the molecular mechanisms underlying the development of pancreatic cancer with the hope that this will lead to preventative and treatment strategies to improve the outcome of the disease. Numerous factors contribute to progression of this disease, including constitutively active NFκB, which has been shown to positively influence cancer cell survival, proliferation, invasion, metastasis and chemoresistance. Recently, the cytoplasmic serine/threonine protein kinase glycogen synthase kinase-3β (GSK-3β) was found to regulate NFκB activation and the proliferation and survival of pancreatic cancer cells. Moreover, recent studies in other human malignancies have implicated GSK-3β as a regulator of cancer cell proliferation, survival and chemoresistance through distinct mechanisms. Thus, GSK-3β has emerged as a viable therapeutic target in the treatment of several human neoplasms.",
keywords = "β-Catenin, Glycogen synthase, Glycogen synthase kinase-3, Heterochromatin, NFκB, Pancreatic adenocarcinoma",
author = "Billadeau, {Daniel D}",
year = "2007",
month = "10",
doi = "10.1159/000108955",
language = "English (US)",
volume = "7",
pages = "398--402",
journal = "Pancreatology",
issn = "1424-3903",
publisher = "S. Karger AG",
number = "5-6",

}

TY - JOUR

T1 - Primers on molecular pathways

T2 - The glycogen synthase kinase-3β

AU - Billadeau, Daniel D

PY - 2007/10

Y1 - 2007/10

N2 - Despite tremendous scientific effort, conventional treatment approaches have had little impact on the course of pancreatic ductal adenocarcinoma. Therefore, urgency is needed to understand the molecular mechanisms underlying the development of pancreatic cancer with the hope that this will lead to preventative and treatment strategies to improve the outcome of the disease. Numerous factors contribute to progression of this disease, including constitutively active NFκB, which has been shown to positively influence cancer cell survival, proliferation, invasion, metastasis and chemoresistance. Recently, the cytoplasmic serine/threonine protein kinase glycogen synthase kinase-3β (GSK-3β) was found to regulate NFκB activation and the proliferation and survival of pancreatic cancer cells. Moreover, recent studies in other human malignancies have implicated GSK-3β as a regulator of cancer cell proliferation, survival and chemoresistance through distinct mechanisms. Thus, GSK-3β has emerged as a viable therapeutic target in the treatment of several human neoplasms.

AB - Despite tremendous scientific effort, conventional treatment approaches have had little impact on the course of pancreatic ductal adenocarcinoma. Therefore, urgency is needed to understand the molecular mechanisms underlying the development of pancreatic cancer with the hope that this will lead to preventative and treatment strategies to improve the outcome of the disease. Numerous factors contribute to progression of this disease, including constitutively active NFκB, which has been shown to positively influence cancer cell survival, proliferation, invasion, metastasis and chemoresistance. Recently, the cytoplasmic serine/threonine protein kinase glycogen synthase kinase-3β (GSK-3β) was found to regulate NFκB activation and the proliferation and survival of pancreatic cancer cells. Moreover, recent studies in other human malignancies have implicated GSK-3β as a regulator of cancer cell proliferation, survival and chemoresistance through distinct mechanisms. Thus, GSK-3β has emerged as a viable therapeutic target in the treatment of several human neoplasms.

KW - β-Catenin

KW - Glycogen synthase

KW - Glycogen synthase kinase-3

KW - Heterochromatin

KW - NFκB

KW - Pancreatic adenocarcinoma

UR - http://www.scopus.com/inward/record.url?scp=35348826780&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35348826780&partnerID=8YFLogxK

U2 - 10.1159/000108955

DO - 10.1159/000108955

M3 - Article

C2 - 17912008

AN - SCOPUS:35348826780

VL - 7

SP - 398

EP - 402

JO - Pancreatology

JF - Pancreatology

SN - 1424-3903

IS - 5-6

ER -