Background: Malignant gliomas are lethal cancers, highly dependent on angiogenesis and treatment options and prognosis still remain poor for patients with recurrent glioblastoma multiforme (GBM). Ephs and ephrins have many well-defined functions during embryonic development of central nervous system such as axon mapping, neural crest cell migration, hindbrain segmentation and synapse formation as well as physiological and abnormal angiogenesis. Accumulating evidence indicates that Eph and ephrins are frequently overexpressed in different tumor types including GBM. However, their role in tumorigenesis remains controversial, as both tumor growth promoter and suppressor potential have been ascribed to Eph and ephrins while the function of EphA7 in GBM pathogenesis remains largely unknown.

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Abstract. The aim of this study was to investigate the difference in gene expression profiles of human lung adenocarcinoma cells and identify genes whose expression is altered by heavy ions but not X-rays. The lung adenocarcinoma cell line A549 was irradiated with carbon ion beams and X-rays using biologically equivalent doses (2 Gy and 6 Gy, respectively). The transcriptional profiling was determined with a high density cDNA microarray containing 11.800 genes, and genetic network and gene ontology analysis was performed. The changes in selected genes involved were validated by quantitative real-time polymerase chain reaction (qRT-PCR). The microarray analysis identified 49 mapped, network-eligible genes, the expression level of which was altered by carbon ions but not by X-rays. From these, 29 were upregulated while 20 genes were downregulated 4 h postirradiation with carbon ions in A549 cells, as compared to the control. Among these, three genes (CCND2, RARG and E2F5) were involved in the aryl hydrocarbon receptor signalling and G1/S cell cycle checkpoint pathways. The microarray data were corroborated by qRT-PCR analysis of the selected genes (p<0.05). Our findings provide information on the genetic signature of carbon ions in human lung adenocarcinoma cells and add to the understanding of the complicated molecular response to carbon ion irradiation.

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