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首页> 外文期刊>Cellular Physiology and Biochemistry >Chloride ion modulates cell proliferation of human androgen-independent prostatic cancer cell
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Chloride ion modulates cell proliferation of human androgen-independent prostatic cancer cell

机译：氯离子调节非雄激素依赖性前列腺癌细胞的细胞增殖

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摘要

In the present study, we investigated if the intracellular Cl~- affects cell growth and cell cycle progression of androgen-independent prostate cancer PC3 cells. PC3 cells cultured in a medium containing 113 mM Cl ~- for 96 h grew up 9-fold in cell number, while PC3 cells cultured in an 8 mM-Cl~--containing culture medium showed complete arrest of cell growth even after culture for 96 h. Exposure of cells to the 8 mM-Cl ~- culture medium diminished phosphorylation levels of Rb and cdc2, which are respectively key accelerators of transition from G_1 to S phase and G_2 to M phase in cell cycle progression. Culturing cells in the 8 mM-CI~--containing culture medium upregulated the protein expression level of p21 (a CDK inhibitor) inhibiting transition of G_1 to S phase, and diminished the incorporation of 5-ethynyl-2′-deoxyuridine (EdU; a thymidine analogue) into DNA. These results suggest that cells cultured in the low Cl~- medium prolonged the duration of all phases of the cell cycle (G_1, S, and G_2/M), thereby abolishing overall cell cycle progression. Effects of culturing cells in the low Cl~- culture medium on cell cycle progression would be mediated via a change in the intracellular Cl~- concentration ([Cl~-]_i), since [Cl~-]_i was decreased under a low Cl~- culture medium. To clarify this possibility, we studied effects of furosemide and bumetanide, Na~+/K~+/2Cl~- cotransporter (NKCC) inhibitors, on proliferation of PC3 cells. Furosemide and bumetanide decreased [Cl~-]_i and cell growth of PC3 cells. These results suggest that a change in [Cl~-]_i would play a critical role in this growth mechanism.
机译：在本研究中，我们调查了细胞内Cl〜-是否影响雄激素非依赖性前列腺癌PC3细胞的细胞生长和细胞周期进程。在含有113 mM Cl〜-的培养基中培养96 h的PC3细胞的细胞数目增长了9倍，而在含有8 mM Cl〜-的培养基中培养的PC3细胞甚至在培养3 d后仍能完全阻止细胞生长。 96小时将细胞暴露于8 mM-Cl--培养基中可减少Rb和cdc2的磷酸化水平，Rb和cdc2分别是细胞周期进程中从G_1转变为S期和从G_2转变为M期的关键促进剂。在含有8 mM-Cl〜的培养基中培养的细胞上调了抑制G_1向S期转变的p21（CDK抑制剂）的蛋白表达水平，并减少了5-乙炔基2′-脱氧尿苷（EdU;胸苷类似物）转化成DNA这些结果表明，在低Cl-培养基中培养的细胞延长了细胞周期所有阶段（G_1，S和G_2 / M）的持续时间，从而取消了整个细胞周期进程。在低Cl〜-培养基中培养细胞对细胞周期进程的影响将通过细胞内Cl〜-浓度（[Cl〜-] _ i）的变化来介导，因为[Cl〜-] _ i在低温下会降低。 Cl〜-培养基。为了阐明这种可能性，我们研究了呋塞米和布美他尼，Na〜+ / K〜+ / 2Cl〜-共转运蛋白（NKCC）抑制剂对PC3细胞增殖的影响。速尿和布美他尼降低[Cl〜-] _ i和PC3细胞的细胞生长。这些结果表明[Cl〜-] _ i的变化将在这种生长机制中起关键作用。

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