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Glycogen synthase kinase 3 beta: can it be a target for oral cancer
1Dept, of Molecular Pharmacology and Therapeutics, Loyola University Medical Center, 2160 South First Avenue, Bldg 102, Maywood, IL-60153, USA. mishrark1@yahoo.co.in
Abstract:
Despite progress in treatment approaches for oral cancer, there has been only modest improvement in patient outcomes in the past three decades. The frequent treatment failure is due to the failure to control tumor recurrence and metastasis. These failures suggest that new targets should be identified to reverse oral epithelial dysplastic lesions. Recent developments suggest an active role of glycogen synthase kinase 3 beta (GSK3 beta) in various human cancers either as a tumor suppressor or as a tumor promoter. GSK3beta is a Ser/Thr protein kinase, and there is emerging evidence that it is a tumor suppressor in oral cancer. The evidence suggests a link between key players in oral cancer that control transcription, accelerated cell cycle progression, activation of invasion/metastasis and anti-apoptosis, and regulation of these factors by GSK3beta. Moreover, the major upstream kinases of GSK3beta and their oncogenic activation by several etiological agents of oral cancer support this hypothesis. In spite of all this evidence, a detailed analysis of the role of GSK3beta in oral cancer and of its therapeutic potential has yet to be conducted by the scientific community. The focus of this review is to discuss the multitude of roles of GSK3beta, its possible role in controlling different oncogenic events and how it can be targeted in oral cancer.
Insights
Glycogen synthase kinase 3 beta (GSK3beta) may be a key tumor suppressor in oral cancer. Targeting GSK3beta could offer new therapeutic strategies to combat oral epithelial dysplastic lesions and improve patient outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Oral cancer treatment has seen limited progress in improving patient outcomes over the last 30 years.
- Tumor recurrence and metastasis are primary reasons for treatment failure in oral cancer.
- New therapeutic targets are needed to reverse oral epithelial dysplastic lesions.
Purpose of the Study:
- To review the multifaceted roles of glycogen synthase kinase 3 beta (GSK3beta) in oral cancer.
- To explore the potential of GSK3beta as a therapeutic target for oral cancer.
- To analyze the link between GSK3beta and key oncogenic events in oral cancer.
Main Methods:
- Literature review of existing research on GSK3beta in human cancers.
- Analysis of evidence linking GSK3beta to transcription, cell cycle, invasion, metastasis, and apoptosis in oral cancer.
- Examination of upstream kinases regulating GSK3beta activity and their role in oral cancer etiology.
Main Results:
- Emerging evidence suggests GSK3beta acts as a tumor suppressor in oral cancer.
- GSK3beta may regulate critical oncogenic pathways including transcription, cell cycle progression, invasion, metastasis, and apoptosis.
- Upstream kinases activating GSK3beta are implicated in oral cancer development.
Conclusions:
- GSK3beta plays a significant role in oral cancer development and progression.
- Targeting GSK3beta presents a promising therapeutic avenue for oral cancer.
- Further research is warranted to fully elucidate GSK3beta's role and therapeutic potential in oral cancer.
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