Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/107485
Title: Reduction of equilibrative nitrobenzylthioinosine-sensitive nucleoside transporter in tamoxifen-treated MCF-7 cells: An oestrogen-reversible phenomenon
Authors: Goh, L-B.
Lee, C-W. 
Issue Date: 1997
Source: Goh, L-B.,Lee, C-W. (1997). Reduction of equilibrative nitrobenzylthioinosine-sensitive nucleoside transporter in tamoxifen-treated MCF-7 cells: An oestrogen-reversible phenomenon. Biochemical Journal 327 (1) : 31-36. ScholarBank@NUS Repository.
Abstract: MCF-7 cells display both nitrobenzylthioinosine (NBMPR)-sensitive (es) and NBMPR-insensitive (ei) equilibrative, but not the Na+-dependent, nucleoside transport. Transport of uridine by es is more sensitive to inhibition by purine nucleosides, whereas the ei component is more sensitive to nucleosides without an amino side group, such as inosine and thymidine. When exposed to 10 μM tamoxifen for 5 days, MCF-7 cells displayed a 44% decrease in the total number of NBMPR-binding sites [B(max) from 245000 ± 18000 to 136000 ± 25000 sites per cell (mean ± S.E.M.; n = 5; P < 0.05)], and a 57% decrease in cell growth with no significant change in binding affinities [K(d) from 0.37 ± 0.05 to 0.45 ± 0.08 nM (n = 5; P > 0.05)]. Kinetic studies of [3H]uridine transport showed a decrease in the V(max) of the es component from 21.7 ± 0.3 (n = 8) to 8.4 ± 2.2 μM/s (n = 4; P < 0.05), whereas the V(max) of the ei component [from 4.7 ± 0.5 (n = 8) to 5.8 ± 1.6 μM/s (n = 4; P > 0.05)] and K(m) values for both components [es from 460 ± 80 to 630 ± 280 μM (n ≤ 3; P > 0.05) and ei from 355 ± 115 to 440 ± 220 μM (n ≤ 4; P > 0.05)] did not change significantly. Oestradiol at 100 μM reversed almost completely the NBMPR-binding site decrease and growth retardation in tamoxifen-treated cells. Thus tamoxifen is shown to cause an oestrogen-reversible decrease of es nucleoside transporters in MCF-7 cells.
Source Title: Biochemical Journal
URI: http://scholarbank.nus.edu.sg/handle/10635/107485
ISSN: 02646021
Appears in Collections:Staff Publications

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