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Downregulation of TCEAL7 expression induces CCND1 expression in non-small cell lung cancer

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Abstract

Transcription Elongation Factor A-like 7 (TCEAL7) was first reported as a candidate tumor suppressor gene because of its inactivation in ovarian cancer as a result of promoter methylation. Down-regulation of the TCEAL7 gene expression was also associated with other cancers such as endometrial, breast, brain, prostate, gastric cancers, glioblastoma and linked to tumor phenotypes and clinical outcomes. However, there is no report in the literature investigating the role of TCEAL7 in non-small cell lung cancer. Cyclin D1 is an important molecule in the transition from G1 to S phase of the cell cycle, and is frequently deregulated in cancers. Cylin D1 (CCND1) gene is amplified or overexpressed in a variety of tumors. In our previous study we reported that CCND1 over-expression was not associated with amplification in non-small cell lung cancer. Recently, it has been reported that TCEAL7 regulates CCND1 expression through myc-binding E-box sequences. The aim of this study was to investigate the expression of TCEAL7 gene in non-small cell lung cancer and to determine its effect on the CCND1 expression level. For this purpose, expression levels of TCEAL7 and CCND1 genes were investigated in 50 patients with non-small cell lung cancer by quantitative real time polymerase chain reaction (qRT-PCR). TCEAL7 was under-expressed (68%) in non-small cell lung cancer tumor tissues while CCND1 was over-expressed (42%). The TCEAL7 levels negatively correlated with increased CCND1 expression (p = 0.002).

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Funding

This study was funded by Istanbul University with the Grant Number 21387.

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Correspondence to Nur Buyru.

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The authors declare that they have no conflict of interests.

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The Ethics Committee of Istanbul University, Cerrahpasa Medical Faculty, approved the study (No: 84996).

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Orhan, C., Bulut, P., Dalay, N. et al. Downregulation of TCEAL7 expression induces CCND1 expression in non-small cell lung cancer. Mol Biol Rep 46, 5251–5256 (2019). https://doi.org/10.1007/s11033-019-04982-6

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  • DOI: https://doi.org/10.1007/s11033-019-04982-6

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