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001-es BibID:	BIBFORM001045
Első szerző:	Deli Tamás (szülész-nőgyógyász, endokrinológus szakorvos)
Cím:	Functional genomics of calcium channels in human melanoma cells / Deli T., Varga N., Ádám A., Kenessey I., Rásó E., Puskás L. G., Tóvári J., Fodor J., Sztretye M., Szigeti Gy. P., Csernoch L., Tímár J.
Dátum:	2007
ISSN:	0020-7136 (Print)
Megjegyzések:	Ca(2+)-signaling of human melanoma is in the focus of intensive research since the identification of the role of WNT-signaling in melanomagenesis. Genomic and functional studies pointed to the important role of various Ca(2+) channels in melanoma, but these data were contradictory. In the present study we clearly demonstrate, in a number of different ways including microarray analysis, DNA sequencing and immunocytochemistry, that various human melanoma cell lines and melanoma tissues overexpress ryanodine receptor type 2 (RyR2) and express P2X(7) channel proteins as compared to melanocytes. These channels, although retain some of their usual characteristics and pharmacological properties, display unique features in melanoma cells, including a functional interaction between the two molecules. Unlike P2X(7), RyR2 does not function as a calcium channel. On the other hand, the P2X(7) receptor has an antiapoptotic function in melanoma cells, since ATP-activation suppresses induced apoptosis, while knock down of the gene expression significantly enhances that.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	International Journal of Cancer. - 121 (2007), p. 55-65. -
További szerzők:	Varga Norbert (orvos) Ádám Attila Kenessey István Rásó Erzsébet Puskás László G. Tóvári József Fodor János (1973-) (élettanász, biotechnológus) Sztretye Mónika (1981-) (élettanász, elektrofiziológus) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Csernoch László (1961-) (élettanász) Timár József
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001-es BibID:	BIBFORM125834
Első szerző:	Tímár József
Cím:	Genomics of calcium signaling in human melanoma / József Tímár, Erzsebet Raso, Tamás Deli, László Csernoch
Dátum:	2006
ISSN:	0008-5472 1538-7445
Megjegyzések:	Melanoma is one of the most aggressive human cancer which can colonize the host from a very small primary. On the other hand, melanoma is characterized by an apoptosis-resistant pheno-genotype resulting in resistance to chemotherapy. We have used DNA microarray technology to profile human melanoma compared to benign tumor (nevi) and metastatic variants to non-metastatic ones to reveal genetic background of its geno-phenotype. For this purpose we have used 3 genetically distinct human melanoma cell lines grown in vitro and in vivo. Data indicated that during progression of melanocytes toward melanoma several genes involved in calcium signaling were found to be upregulated including the ryanodin receptor-2 (RYR2), P2X7R and sorcin. During the metastatic progression, beside further upregulation of the P2X7R receptor another set of calcium-signaling genes were found to be upregulated such as T-type Ca-channel-1, sorting nexin and calneuron-1. Functional studies revealed that the RYR2 is not involved directly in Ca-signaling which is predominantly mediated by the purinergic P2X7R receptor. Activation of the RYR2 resulted in stimulation of cell proliferation, while activation of P2X7R by ATP inhibited apoptosis. On the other hand, P2X7R inhibition by Zn++ induced strong inhibition of cell proliferation of human melanoma cell lines partialy mediated by induction of apoptosis. These studies provide the first evidences for the crucial role for calcium signaling in the progression of human melanoma and may provide novel therapeutic targets.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idézhető absztrakt folyóiratcikk genomics calcium signaling human melanoma ryanodine receptor P2X7 purinergic receptor
Megjelenés:	Cancer Research. - 66 : Supplement 8 (2006), p. 982. -
További szerzők:	Rásó Erzsébet Deli Tamás (1979-) (szülész-nőgyógyász, endokrinológus szakorvos) Csernoch László (1961-) (élettanász)
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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