Protein tyrosine phosphorylation is a crucial signaling mechanism that plays a role in epithelial carcinogenesis.
Protein tyrosine kinases (PTKs) control various cellular processes including growth, differentiation,
metabolism, and motility by activating major signaling pathways including STAT3, AKT, and MAPK. Genetic
mutation of PTKs and/or prolonged activation of PTKs and their downstream pathways can lead to the development
of epithelial cancer. Therefore, PTKs became an attractive target for cancer prevention. PTK inhibitors are
continuously being developed, and they are currently used for the treatment of cancers that show a high expression
of PTKs. Protein tyrosine phosphatases (PTPs), the homeostatic counterpart of PTKs, negatively regulate the
rate and duration of phosphotyrosine signaling. PTPs initially were considered to be only housekeeping enzymes
with low specificity. However, recent studies have demonstrated that PTPs can function as either tumor suppressors
or tumor promoters, depending on their target substrates. Together, both PTK and PTP signal transduction
pathways are potential therapeutic targets for cancer prevention and treatment.
Keywords: Carcinogenesis, tyrosine phosphorylation, PTK, PTP, EGFR, IGF-1R, STAT3, AKT.
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