Expression of E1AF, an ets-family transcription factor, is correlated with the invasive phenotype of oral squamous cell carcinoma.
ABSTRACT E1AF is a newly identified ets-oncogene family transcription factor. Previous reports have noted that E1AF can upregulate promoter activities of several matrix metalloproteinase (MMP) genes and showed that invasive potentials of oral squamous cell carcinoma-derived cell lines are correlated with expression of E1AF and MMPs. The invasive phenotype is restrained by transfection with an antisense E1AF expression vector. Thus, E1AF is thought to be highly correlated with malignant potentials of cancer cells. However, little is known about E1AF expression and cancer cell malignancies in in vivo tumours. In the present study, 27 oral squamous cell carcinoma (SCC) specimens were examined using RT-PCR, Southern blot hybridisation and in situ hybridisation (ISH) and compared to the clinicopathological parameters. Among the 27 patients, E1AF was detected in 15 cases. E1AF mRNA was detected in 13 of 17 invasive SCCs, whereas the majority of SCCs not expressing E1AF showed an expansive growth pattern. Increased prevalence of E1AF-positive oral SCC was observed in cases with nodal metastasis. These results indicate that E1AF may be involved in cancer cell malignancies through its ability to promote invasive potential.
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ABSTRACT: Multiple gene disorders have been shown to be involved in carcinogenesis. Mutation, translocation and amplification have been identified in so-called oncogenes, and inactivation of antioncogenes by mutation and deletion has been shown. E1AF is an ets-oncogene family transcription factor, and has been shown to upregulate multiple matrix metalloproteinase (MMP) genes that contribute to the malignant phenotype of cancer cells by inducing invasive and metastatic activities. EWS/ETS fusions are frequently observed in Ewing's sarcoma, and we have revealed that EWS/ETS chimeric protein activates telomerase activity by upregulating human telomerase reverse transcriptase (hTERT), but the transcriptional activation of hTERT by EWS/ETS was indirect, and EWS/ETS was seen to function as a co-activator for TERT transcription. A number of oncogenes and cancer-related genes contain AU-rich element (ARE) in non-coding regions of transcribed mRNA. HuR is a RNA-binding protein that has the potential to stabilize ARE-containing mRNAs. HuR is known to shuttle between the nucleus and the cytoplasm via several export pathways. When normal cells are exposed to stress, HuR is exported to the cytoplasm in a chromosome maintenance region 1 (CRM1)-dependent manner. However, we demonstrate that HuR is CRM-1 independently exported to the cytoplasm in oral cancer cells. ARE-mRNAs were also exported to the cytoplasm and stabilized in the oral cancer cells, which were inhibited by HuR knockdown. These findings suggest that transcriptional and translational abnormalities of oncogenes may contribute to the carcinogenesis of oral epithelial cells.International Journal of Oral Science 05/2010; 7(1):11–18. DOI:10.1016/S1348-8643(10)80008-4 · 2.03 Impact Factor