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Glycogen synthase kinase-3β: a novel therapeutic target for pancreatic cancer

Li Ding1, Daniel D Billadeau1

  • 1The Division of Oncology Research, Schulze Center for Novel Therapeutics, Mayo Clinic, Rochester, MN, USA.

Expert Opinion on Therapeutic Targets
|March 18, 2020
PubMed

Insights

Glycogen synthase kinase-3β (GSK-3β) is overexpressed in pancreatic ductal adenocarcinoma (PDAC), driving tumor progression and chemoresistance. Inhibiting GSK-3β alongside chemotherapy shows promise for treating this deadly cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis, necessitating novel therapeutic targets.
  • Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine kinase implicated in cancer development.
  • GSK-3β is overexpressed in PDAC and contributes to tumor progression, survival, and chemoresistance.

Purpose of the Study:

  • To review the regulatory mechanisms of GSK-3β activity in PDAC.
  • To summarize the downstream targets and functions of GSK-3β in PDAC.
  • To discuss the therapeutic potential of targeting GSK-3β in PDAC.

Main Methods:

  • Literature review of studies on GSK-3β regulation and function in PDAC.
  • Analysis of upstream regulatory pathways (translational, post-translational).
  • Examination of downstream targets involved in PDAC cell growth, metastasis, and chemoresistance.

Main Results:

  • Oncogenic KRas upregulates GSK-3β expression in PDAC.
  • GSK-3β regulates key pathways controlling cancer cell proliferation and survival.
  • GSK-3β contributes to resistance against chemotherapy agents.

Conclusions:

  • GSK-3β is a critical mediator of PDAC progression and therapeutic resistance.
  • Targeting GSK-3β activity presents a viable strategy for PDAC treatment.
  • Combination therapy with GSK-3β inhibitors and chemotherapeutics may improve patient outcomes.
Keywords:
GSK-3GSK-3 inhibitorsKRaspancreatic cancerpancreatic ductal adenocarcinomatargeted therapy

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