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. 2020 Nov 13;17(1):207-217.
doi: 10.5114/aoms.2020.100780. eCollection 2021.

Prognostic value of the PIK3CA, AKT, and PTEN mutations in oral squamous cell carcinoma: literature review

Anna Starzyńska  1 , Aleksandra Sejda  2 , Paulina Adamska  1 , Giulia Marvaso  3   4 , Monika Sakowicz-Burkiewicz  5 , Łukasz Adamski  1 , Barbara A Jereczek-Fossa  3   4
Affiliations

Prognostic value of the PIK3CA, AKT, and PTEN mutations in oral squamous cell carcinoma: literature review

Anna Starzyńska et al. Arch Med Sci. .

Abstract

Over 260,000 (2013) new oral squamous cell carcinoma (OSCC) cases are reported annually worldwide. Despite development in OSCC management, the outcome is still unsatisfactory. Identification of new molecular markers may be of use in prevention, prognosis, and choice of an appropriate therapy. The intracellular molecular signalling pathway of phosphatidyl-inositol-3-kinase is involved in the process of cell growth, differentiation, migration, and survival. The main components of this pathway: PIK3CA (phosphatidylinositol-4,5-bisphosphate-3-kinase catalytic subunit α), PTEN (phosphatase and tensin homologue deleted on chromosome 10), and AKT (serine-threonine kinase) are potential objects of research when introducing new therapeutic agents. The aim of this paper is to evaluate the PIK3CA, PTEN, and AKT gene mutations as prognostic factors in OSCC and to describe their role in aggressive disease progression. This is crucial for oral cancer biology understanding and for indicating which direction new clinical treatments should take.

Keywords: AKT; PIK3CA; PTEN; oral squamous cell carcinoma.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Diagram of phosphatidyl-inositol 3-kinase/serine-threonine kinase pathway. Receptor tyrosine kinase activates phosphatidyl-inositol 3-kinase catalytic subunit p110 and regulatory subunit p85 that converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol 3,4,5-trisphosphate and causes serine-threonine kinase membrane recruitment and activation, and hence regulating transcription in the cell nucleus RTK – receptor tyrosine kinase, PTEN – phosphatase and tensin homologue encoded on chromosome 10, PIP2 – phosphatidylinositol 4,5-bisphosphate, PIP3 – phosphatidylinositol 3,4,5-trisphosphate, PDK1 – 3-phosphoinositide-dependent kinase-1, PP2A – protein phosphatase 2, PH – pleckstrin homology domain, AKT – serine-threonine kinase, T308 –threonine 308 phosphorylation site at the AKT kinase catalytic domain, S473 – serine 473 phosphorylation site at the AKT kinase regulatory domain, PO4 – phosphate group, VEGF – vascular endothelial growth factor, p85 – regulatory domain of phosphatidyl-inositol 3-kinase, p110 – catalytic domain of phosphatidyl-inositol 3-kinase, PTEN – phosphatase and tensin homologue protein acts as a phosphatase to dephosphorylate, PIP3 – this dephosphorylation results in inhibition of the AKT signalling pathway.
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