Transcriptomic dissection of tongue squamous cell carcinoma.

BMC Genomics

Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, IL, USA.

Published: February 2008

AI Article Synopsis

  • The study focuses on oral tongue squamous cell carcinoma (OTSCC), a highly aggressive type of head and neck cancer that varies in risk factors and genetic traits.
  • Genome-wide analysis of 53 primary OTSCCs and 22 normal tissues identified several genes with significant expression differences, including up-regulated (e.g., MMP1, IL8) and down-regulated genes (e.g., KRT4, MAL).
  • The findings suggest altered biological processes in OTSCC, which might aid in developing diagnostic tools and guide further research into targeted gene functions for this aggressive cancer type.

Article Abstract

Background: The head and neck/oral squamous cell carcinoma (HNOSCC) is a diverse group of cancers, which develop from many different anatomic sites and are associated with different risk factors and genetic characteristics. The oral tongue squamous cell carcinoma (OTSCC) is one of the most common types of HNOSCC. It is significantly more aggressive than other forms of HNOSCC, in terms of local invasion and spread. In this study, we aim to identify specific transcriptomic signatures that associated with OTSCC.

Results: Genome-wide transcriptomic profiles were obtained for 53 primary OTSCCs and 22 matching normal tissues. Genes that exhibit statistically significant differences in expression between OTSCCs and normal were identified. These include up-regulated genes (MMP1, MMP10, MMP3, MMP12, PTHLH, INHBA, LAMC2, IL8, KRT17, COL1A2, IFI6, ISG15, PLAU, GREM1, MMP9, IFI44, CXCL1), and down-regulated genes (KRT4, MAL, CRNN, SCEL, CRISP3, SPINK5, CLCA4, ADH1B, P11, TGM3, RHCG, PPP1R3C, CEACAM7, HPGD, CFD, ABCA8, CLU, CYP3A5). The expressional difference of IL8 and MMP9 were further validated by real-time quantitative RT-PCR and immunohistochemistry. The Gene Ontology analysis suggested a number of altered biological processes in OTSCCs, including enhancements in phosphate transport, collagen catabolism, I-kappaB kinase/NF-kappaB signaling cascade, extracellular matrix organization and biogenesis, chemotaxis, as well as suppressions of superoxide release, hydrogen peroxide metabolism, cellular response to hydrogen peroxide, keratinization, and keratinocyte differentiation in OTSCCs.

Conclusion: In summary, our study provided a transcriptomic signature for OTSCC that may lead to a diagnosis or screen tool and provide the foundation for further functional validation of these specific candidate genes for OTSCC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2262071PMC
http://dx.doi.org/10.1186/1471-2164-9-69DOI Listing

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