Expression analysis of genes at 3q26-q27 involved in frequent amplification in squamous cell lung carcinoma

• Published in: European journal of cancer (1990) 1999-04, Vol.35 (4), p.641-646
• Main Authors: Rácz, A., Brass, N., Heckel, D., Pahl, S., Remberger, K., Meese, E.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Blotting, Southern; Carcinoma, Squamous Cell - genetics; chromosomal band 3q26-q27; Chromosomes, Human, Pair 3 - genetics; Gene Amplification; gene expression; Gene Expression Regulation, Neoplastic - genetics; Humans; Lung Neoplasms - genetics; Medical sciences; Pneumology; Reverse Transcriptase Polymerase Chain Reaction; squamous cell lung carcinoma (SCC); Tumors of the respiratory system and mediastinum
• ISSN: 0959-8049; 1879-0852
• DOI: 10.1016/S0959-8049(98)00419-5

Gene amplifications are known to occur frequently in lung cancer. Recently, we identified gene amplifications at 3q26 in squamous cell lung carcinoma (SCC) using reverse chromosome painting. Here, our aim was to analyse the expression of genes which map within the amplified chromosomal region. The genes which were selected for their known function and their potential involvement in tumour development included the genes for ribosomal protein L22 ( RPL22), butyrylcholinesterase ( BCHE), glucose transporter 2 ( SLC2A2), transferrin receptor ( TFRC), thrombopoietin ( THPO) and the phosphatidylinositol-3 kinase catalytic alpha polypeptide ( PIK3CA). While five genes were expressed in the majority of the 17 samples of SCC, the gene for the glucose transporter 2 ( SLC2A2) was expressed in only three cases, excluding SLC2A2 as the target gene of the amplification unit. For a subset of tumours, we determined the amplification status of the six genes. The TFRC, PIK3CA, BCHE, THPO and SLC2A2 genes were amplified in several cases, whereas the RPL22 gene was amplified in only one case. The combined amplification and expression data of this and our previous studies indicate that the amplified region at 3q26 contains several genes that are transcribed in SCC, providing the possibility that several amplified and functionally important genes at 3q26 may be involved in the pathogenesis of SCC.