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. 2016 Apr;11(4):2913-2918.
doi: 10.3892/ol.2016.4309. Epub 2016 Mar 8.

Analysis of PI3K pathway components in human cancers

Jamila Daragmeh  1 , Waseim Barriah  2 , Bashar Saad  3 , Hilal Zaid  3
Affiliations

Analysis of PI3K pathway components in human cancers

Jamila Daragmeh et al. Oncol Lett. 2016 Apr.

Abstract

Recent advances in genomics, proteomics, cell biology and biochemistry of tumors have revealed new pathways that are aberrantly activated in numerous cancer types. However, the enormous amount of data available in this field may mislead scientists in focused research. As cancer cell growth and progression is often dependent upon the phosphoinositide 3-kinase (PI3K)/AKT pathway, there has been extensive research into the proteins implicated in the PI3K pathway. Using data available in the Human Protein Atlas database, the current study investigated the expression of 25 key proteins that are known to be involved with PI3K pathway activation in a distinct group of 20 cancer types. These proteins are AKTIP, ARP1, BAD, GSK3A, GSK3B, MERTK-1, PIK3CA, PRR5, PSTPIP2, PTEN, FOX1, RHEB, RPS6KB1, TSC1, TP53, BCL2, CCND1, WFIKKN2, CREBBP, caspase-9, PTK2, EGFR, FAS, CDKN1A and XIAP. The analysis revealed pronounced expression of specific proteins in distinct cancer tissues, which may have the potential to serve as targets for treatments and provide insights into the molecular basis of cancer.

Keywords: AKT; EGFR; Human Protein Atlas; PI3K; PTEN; TSC1; cancer; tumorigenesis.

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Figures

Figure 1.
Figure 1.
PI3K/AKT signaling pathway. Binding of the ligand to membrane receptor tyrosine kinases activates PI3K, which phosphorylates PIP2 to produce PIP3. PIP3 recruits PDK1 to the plasma membrane. PDK1 phosphorylates and activates AKT, which regulates various cellular processes. The lipid phosphate activity of cytoplasmic PTEN dephosphorylates PIP3, thereby decreasing PIP3 levels and increasing levels of PIP2, resulting in a concomitant decrease in AKT activity. PI3K, phosphoinositide 3-kinase; AKT, protein kinase B; PIP2 [PI(4,5)P], phosphatidylinositol 4,5-bisphosphate; PIP3 [PI(3,4,5)P], phosphatidylinositol (3,4,5)-trisphosphate; PDK1, phosphoinositide-dependent kinase 1; PTEN, phosphatase and tensin homolog.
Figure 2.
Figure 2.
Expression levels of tuberous sclerosis 1 (TSC1) protein in different cancer tissues based on Human Protein Atlas.
Figure 3.
Figure 3.
Expression percentages of epidermal growth factor receptor (EGFR) protein in 10 different cancer tissues based on Human Protein Atlas.
Figure 4.
Figure 4.
Expression percentages of MER proto oncogene tyrosine kinase (MERTK) protein in different cancer tissues based on Human Protein Atlas.
Figure 5.
Figure 5.
Expression percentages of Ras homolog enriched in brain (RHEB)protein in different cancer tissues based on Human Protein Atlas.
Figure 6.
Figure 6.
Expression percentages of ribosomal protein S6 β1 (RPS6KB1) protein in different cancer tissues based on Human Protein Atlas.
Figure 7.
Figure 7.
Expression percentages of Cyclin D1 (CCND1) protein in different cancer tissues based on Human Protein Atlas.
Figure 8.
Figure 8.
Expression percentages of tumor protein p53 (TP53) in different cancer tissues based on Human Protein Atlas.
Figure 9.
Figure 9.
Expression percentages of phosphatase and tensin homolog (PTEN) protein (tumor suppressor gene) based on Human Protein Atlas.
Figure 10.
Figure 10.
Expression percentage of phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (PIK3CA) protein based on Human Protein Atlas.
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