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001-es BibID:	BIBFORM065337
Első szerző:	Xie, Yuntao
Cím:	Gene expression profile by blocking the SYT-SSX fusion gene in synovial sarcoma cells. Identification of XRCC4 as a putative SYT-SSX target gene / Yuntao Xie, Maria Törnkvist, Yan Aalto, Gunnar Nilsson, Leonard Girnita, Bálint Nagy, Sakari Knuutila, Olle Larsson
Dátum:	2003
ISSN:	0950-9232
Megjegyzések:	Increasing evidence suggests that the SYT-SSX fusion gene plays an important role in synovial sarcoma development and progression. However, very little is known about the downstream targets of SYT-SSX. In this study, we used antisense oligonucleotides to block the expression of the SYT-SSX fusion gene in synovial sarcoma cells. By comparing SYT-SSX inhibited cells with noninhibited cells, the gene expression profile was analysed using cDNA microarray and established by real-time PCR. Herewith, using a filter containing 1176 cancer-relevant genes, we found that the DNA repair gene XRCC4 and the DNA mismatch repair gene MSH2 were downregulated, whereas the gene encoding for the serine/threonine protein kinase PRK (also known as CNK), and the macrophage inhibitory cytokine MICI (also known as PLAB) were upregulated after the inhibition of SYT-SSX. In comparison, expression of the XRCC4 gene was undergoing the strongest alteration. Consistently, the protein expression of XRCC4 was found to be decreased after SYT-SSX inhibition, whereas there were no detectable changes for the other gene products. Our study provides some clues to elucidate the signaling pathways of the SYT-SSX fusion gene, as well as it demonstrates a valuable model system for search for other SYT-SSX targets.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban gene expression synovial carcinoma SYT-SSX fusion gene
Megjelenés:	Oncogene. - 22 : 48 (2003), p. 7628-7631. -
További szerzők:	Törnkvist, Maria Aalto, Yan Nilsson, Gunnar Girnita, Leonard Nagy Bálint (1956-) (molekuláris genetikus) Knuutila, Sakari Larsson, Olle
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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