Background: Glycogen syntheis kinase (GSK-3) inhibitors are novel therapeutic agents
for treating various types of cancer, such as breast, lung, and gastric cancer. No pathological
changes have been found by the morphological examination of GSK-3.
Objectives: This review describes recent procedures using GSK-3 inhibitors, primarily in treating
colon carcinoma. Furthermore, it also explains the mechanism of action of different GSK-3 inhibitors
in treating various types of cancers and proposes some additional mechanisms may be useful
for further research on GSK-3 inhibitors for cancers, including colon carcinoma.
Results: The majority of the cancerous and pre-cancerous lesions are stimulated by the transformation
of membrane-bound arachidonic acid (AA) to eicosanoids, a transformation that promotes for
the viability, proliferation, and spread of cancer. GSK-3 inhibitors can reinstate hostility to tumor
necrosis factor-related apoptosis-inducing ligand (TRAIL) responsiveness in gastric adenocarcinoma
cells. GSK-3, the final enzyme in glycogen synthesis, is a serine/threonine kinase that phosphorylates
varied sequences that are more than a hundred in number, within proteins in an array of
heterogeneous pathways. It is an essential module of an exceptionally large number of cellular processes,
playing a fundamental role in many metabolic processes and diseases. Many patients diagnosed
with colon cancer achieve long-term remission with outstanding survival through the GSK-3
Conclusion: Prior to the extensive application of these proposed mechanisms of GSK-3 inhibitor,
further evaluation and clinical studies are needed. Only after the completion of appropriate clinical
studies and morphological examinations, would extensive application be apprpriate.