Multidrug Resistance Reversing Activity of Newly Developed Phenothiazines on P-glycoprotein (ABCB1)-related Resistance of Mouse T-Lymphoma Cells

BACKGROUND: Phenothiazines have anticancer properties and are able to reverse the multidrug resistance of neoplastic cells by inhibiting the ATP-binding cassette, sub-family B (MDR/TAP), member 1 protein (ABCB1 or P-glycoprotein) activity. MATERIALS AND METHODS: A series of new phenothiazine deriva...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Spengler Gabriella
Takács Daniella
Horváth Ádám
Riedl Zsuzsanna
Hajós György
Amaral Leonard
Molnár József
Dokumentumtípus: Cikk
Megjelent: 2014
Sorozat:ANTICANCER RESEARCH 34 No. 4
mtmt:2583773
Online Access:http://publicatio.bibl.u-szeged.hu/10441
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520 3 |a BACKGROUND: Phenothiazines have anticancer properties and are able to reverse the multidrug resistance of neoplastic cells by inhibiting the ATP-binding cassette, sub-family B (MDR/TAP), member 1 protein (ABCB1 or P-glycoprotein) activity. MATERIALS AND METHODS: A series of new phenothiazine derivatives was investigated regarding their ABCB1-modulating effect on multidrug resistant mouse T-lymphoma cells by rhodamine 123 accumulation assay and real-time ethidium bromide accumulation assay. RESULTS: The phenothiazine derivatives exhibited a potent anticancer effect on the parental cell line and on its multidrug-resistant mouse T-lymphoma subline overexpressing the ABCB1 transporter. The inhibition of the ABCB1 transporter in the presence of the newly-developed phenothiazines was greater than that for the known ABCB1 inhibitors thioridazine and verapamil. CONCLUSION: Based on the chemical structures and biological activity, compounds with bivalent sulfur atom in the phenothiazine ring demonstrated marked ABCB1-modulating effect, however, other derivatives with halogen or amide substitutions were ineffective. 
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700 0 1 |a Horváth Ádám  |e aut 
700 0 1 |a Riedl Zsuzsanna  |e aut 
700 0 1 |a Hajós György  |e aut 
700 0 1 |a Amaral Leonard  |e aut 
700 0 1 |a Molnár József  |e aut 
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