Genome-wide screening of copy number alterations and LOH events in renal cell carcinomas and integration with gene expression profile

Table 4 Selection of differentially expressed genes potentially involved in RCC pathology.

Gene symbol (chr)	Gene name	Biological function	Differential expression in RCC	References
RGS5 (1q)	Regulator of G-protein signalling 5	angiogenesis	up	[[18, 27]]
CXCR4 (2q)	Chemokine C-X-C receptor 4	metastatic spread	up	[[18, 26]]
LOX (5q)	Lysyl oxidase	metastatic spread	up	[[18, 27]]
VEGFA (6p)	Vascular endothelial growth factor A	angiogenesis	up	[[18, 26]]
CAV1 (7q)	Caveolin 1	cell adhesion and extracellular matrix interaction	up	[[18, 41]]
HIG2 (7q)	Hypoxia-inducible protein 2	cell growth promotion	up	[[18, 27, 42]]
CA9 (9p)	Carbonic anhydrase IX	cell growth promotion	up	[[18, 43]]
VIM (10p)	Vimentin	cell adhesion and extracellular matrix interaction	up	[44]
NNMT (11q)	Nicotinamide N-methyltransferase	methyltransferase activity	up	[[18, 45]]
EGLN3 (14q)	Egl nine homolog 3	cell growth regulation	up	[[18, 27]]
DEFB1 (8p)	Defensin beta 1	antimicrobial activity	down	[[44]]
PVALB (22q)	Parvalbumin	calcium ion binding	down	[[44]]

Differentially expressed genes were calculated by SAM analysis comparing 16 RCC tissue samples to 11 normal cortical tissues. Genes were selected by comparing our list with the RCC dataset of Jones et al. and with published literature. References specifically reporting a potential role of these genes in RCC pathology are indicated.

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