Unaltered mRNA Levels of EGFR and PIK3CA in Head and Neck Squamous Cell Carcinoma
Abstract
Background: Since its identification, the Epidermal Growth Factor Receptor (EGFR) signaling pathway through PIK3CA, has been known to be involved in the pathogenesis of several solid tumors especially Head and Neck Squamous Cell Carcinoma (HNSCC). Impaired signal transduction through EGFR-PIK3CA may give rise to oncogenic processes because of its key role in regulation of major cellular functions. Several oncogenic mechanisms mediated by unregulated EGFR signaling pathways have been suggested by previous studies including, mutations in genes encoding EGFR and PIK3CA and increased ligands of EGFR. Here, we aimed to compare the total gene expression of EGFR and PIK3CA on mRNA level between HNSCC tissues and normal squamous cell tissues. Methods: In this pilot study, we examined 31 samples of tumor-infected squamous cell tissues as well as 31 samples of healthy tissues around the tumor as controls for the expression of EGFR and PIK3CA genes using quantitative polymerase chain reactions (Q-PCR). Results: both EGFR and PIK3CA mRNA levels were slightly altered in HNSCC tissues compared with the control group (3% decrease and 9% increase respectively) but these differences were not statistically significant. Conclusion: our results indicate that total EGRF and PIK3CA expression in mRNA level is not altered in Head and Neck Squamous Cell Carcinomas compared with that of normal squamous cell tissues.
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20. Morris, L.G., et al., Genomic dissection of the epidermal growth factor receptor (EGFR)/PIK3CA pathway reveals frequent deletion of the EGFR phosphatase PTPRS in head and neck cancers. Proceedings of the National Academy of Sciences, 2011. 108(47): p. 19024-19029.
2. Shibuya, K., et al., Global and regional estimates of cancer mortality and incidence by site: II. Results for the global burden of disease 2000. BMC cancer, 2002. 2(1): p. 37.
3. Gillison, M.L., et al., Distinct risk factor profiles for human papillomavirus type 16–positive and human papillomavirus type 16–negative head and neck cancers. Journal of the National Cancer Institute, 2008. 100(6): p. 407-420.
4. Decker, J. and J.C. Goldstein, Risk factors in head and neck cancer. New England Journal of Medicine, 1982. 306(19): p. 1151-1155.
5. Huang, S.-M. and P.M. Harari, Epidermal growth factor receptor inhibition in cancer therapy: biology, rationale and preliminary clinical results. Investigational new drugs, 1999. 17(3): p. 259-269.
6. Hynes, N., et al., The ErbB receptor tyrosine family as signal integrators. Endocrine-Related Cancer, 2001. 8(3): p. 151-159.
7. Psyrri, A., T.Y. Seiwert, and A. Jimeno. Molecular pathways in head and neck cancer: EGFR, PIK3CA, and more. in American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Meeting. 2013.
8. Zandi, R., et al., Mechanisms for oncogenic activation of the epidermal growth factor receptor. Cellular signalling, 2007. 19(10): p. 2013-2023.
9. Bian, Y., et al., Loss of TGF-β signaling and PTEN promotes head and neck squamous cell carcinoma through cellular senescence evasion and cancer-related inflammation. Oncogene, 2012. 31(28): p. 3322-3332.
10. Chomczynski, P. and N. Sacchi, Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. Analytical biochemistry, 1987. 162(1): p. 156-159.
11. Lemmon, M.A. and J. Schlessinger, Cell signaling by receptor tyrosine kinases. Cell, 2010. 141(7): p. 1117-1134.
12. Hunter, T., Signaling—2000 and beyond. Cell, 2000. 100(1): p. 113-127.
13. Paul, M.K. and A.K. Mukhopadhyay, Tyrosine kinase–role and significance in cancer. International journal of medical sciences, 2004. 1(2): p. 101.
14. Cantley, L.C., The phosphoinositide 3-kinase pathway. Science, 2002. 296(5573): p. 1655-1657.
15. Maurizi, M., et al., Prognostic significance of epidermal growth factor receptor in laryngeal squamous cell carcinoma. British Journal of Cancer, 1996. 74(8): p. 1253-1257.
16. Nicholson, R., J. Gee, and M. Harper, EGFR and cancer prognosis. European journal of cancer, 2001. 37: p. 9-15.
17. Huang, H.-J.S., et al., The enhanced tumorigenic activity of a mutant epidermal growth factor receptor common in human cancers is mediated by threshold levels of constitutive tyrosine phosphorylation and unattenuated signaling. Journal of Biological Chemistry, 1997. 272(5): p. 2927-2935.
18. Lee, J.W., et al., Somatic mutations of EGFR gene in squamous cell carcinoma of the head and neck. Clinical Cancer Research, 2005. 11(8): p. 2879-2882.
19. Vogt, P.K., et al., Cancer-specific mutations in phosphatidylinositol 3-kinase. Trends in biochemical sciences, 2007. 32(7): p. 342-349.
20. Morris, L.G., et al., Genomic dissection of the epidermal growth factor receptor (EGFR)/PIK3CA pathway reveals frequent deletion of the EGFR phosphatase PTPRS in head and neck cancers. Proceedings of the National Academy of Sciences, 2011. 108(47): p. 19024-19029.
| Files | ||
| Issue | Vol 16 No 2 (2024) | |
| Section | Original Articles | |
| DOI | https://doi.org/10.18502/bccr.v16i2.19427 | |
| Keywords | ||
| HNSCC EGFR PIK3CA Carcinoma | ||
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This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
How to Cite
1.
Bafandeh N, Mehrabi S, Parsa H, Zarifian R, Esmaeili M, Shakoori A. Unaltered mRNA Levels of EGFR and PIK3CA in Head and Neck Squamous Cell Carcinoma. Basic Clin Cancer Res. 2025;16(2):79-85.
