Abstract

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 inhibitors.

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.

Keywords: GSK-3 inhibitor, Colon Carcinoma, Colorectal Cancer, OMM, Cancer Cell Apoptosis, DMSO.

Erratum In:
GSK-3 Inhibitors in the Regulation and Control of Colon Carcinoma

Graphical Abstract