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- Title
Down regulation of 3p genes, LTF, SLC38A3 and DRR1, upon growth of human chromosome 3-mouse fibrosarcoma hybrids in severe combined immunodeficiency mice.
- Authors
Kholodnyuk, Irina D.; Kozireva, Svetlana; Kost-Alimova, Maria; Kashuba, Vladimir; Klein, George; Imreh, Stefan
- Abstract
We have applied a functional test for tumour antagonizing genes based on human chromosome 3 (chr3)-mouse fibrosarcoma A9 MCHs that were studied in vitro and after growth as tumours in severe combined immunodeficiency (SCID) mice. Previously, we reported that 9 out of the 36 SCID-tumours maintained the transferred chr3 ('chr3+' tumours), but lost the expression of the known human TSG fragile histidine triad gene ( FHIT) in contrast to 14 other 3p-genes examined. Here we report the results of the duplex RT-PCR analysis of 9 'chr3+' tumours and 3 parental MCHs. We have examined the expression of 34 human 3p-genes from known cancer-related regions of instability, including 13 genes from CER1 defined by us previously at 3p21.33-p21.31 and 10 genes from the LUCA region at 3p21.31. We have found that in addition to FHIT, expression of the LTF gene from CER1 at 3p21.33-p21.31 was lost in all 9 tumours analyzed. The transcript of the solute carrier family 38 member 3 gene ( SLC38A3) gene from LUCA region at 3p21.31 was not found in 8 and was greatly reduced in 1 out of these 9 tumours. Expression of the down-regulated in renal cell carcinoma gene ( DRR1) gene at 3p14.2 was lost in 7 and down regulated in 2 'chr3+' tumours. In the SCID-tumour derived cell lines treatment with 5-aza-2′-deoxycytidine restored the mRNA expression of LTF, indicating the integrity of DNA sequences. Notably that transcription of the LTF and 2 flanking genes, LRRC2 and TMEM7, as well as transcription of the SLC38A3 gene, were also impaired in all 5 RCC cell lines analyzed. Our data indicate these genes as putative tumour suppressor genes. © 2006 Wiley-Liss, Inc.
- Publication
International Journal of Cancer, 2006, Vol 119, Issue 1, p99
- ISSN
0020-7136
- Publication type
Article
- DOI
10.1002/ijc.21794