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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Selective decrease of SN1(SNAT3) mRNA expression in human and rat glioma cells adapted to grow in acidic medium.
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Selective decrease of SN1(SNAT3) mRNA expression in human and rat glioma cells adapted to grow in acidic medium.

机译：SN1（SNAT3）mRNA在人和大鼠胶质瘤细胞适应在酸性介质中生长的选择性降低。

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The system N glutamine (Gln) transporter SN1(SNAT3) is overexpressed in human malignant glioma cells in situ as compared to the adjacent brain tissue or metastases from different organs [Sidoryk, M., Matyja, E., Dybel, A., Zielinska, M., Bogucki, J., Jaskolski, D.J., Liberski, P.P., Kowalczyk, P., Albrecht, J., 2004]. Increased expression of a glutamine transporter SNAT3 is a marker of malignant gliomas. NeuroReport 15, 575-578], but its role in tumor growth as compared to the other Gln transporters is unknown. One of the profound, growth-promoting effects of glial tumor in situ is acidification of the extracellular space. In the kidney SN1(SNAT3) mRNA participates in the adaptation to acidosis. In this study therefore, expression of mRNAs coding for SN1(SNAT3) and other Gln transporters was measured in human (T98G) and rat (C6) glioma cells incubated for 4h in an acidic medium (AI) (pH 6.5). MTT assay revealed no cell loss in AI cells, and intracellular pH (pHi) as measured by a fluorescent probe (BCECF-AM) was slightly alkaline in C6 and T98G cells, indicating that the cells have adapted to AI. AI significantly decreased the SN1(SNAT3) mRNA expression in C6 (a 60% decrease) and T98G cells (a 50% decrease). The decrease retreated in C6 cells 4h after transferring them back to the neutral medium. The expression of ASCT2 mRNA (system ASC), ATA1 mRNA (system A) and SN2(SNAT5) mRNA (system N) were not affected by AI in either of the cell lines. [(3)H]Gln uptake in C6 or T98G cells grown in neutral medium was mainly mediated by system ASCT2: system N contributed to only approximately 7% of the uptake. AI did not affect the total Gln uptake, and only slightly decreased the system N-mediated component of the uptake. Hence, SN1(SNAT3) does not seem to be involved in the adaptation of cultured glioma cells to acidic millieu.
机译：与相邻脑组织或来自不同器官的转移相比，系统N谷氨酰胺（Gln）转运蛋白SN1（SNAT3）在人类恶性神经胶质瘤细胞中过表达[Sidoryk，M.，Matyja，E.，Dybel，A.，Zielinska ，M.，Bogucki，J.，Jaskolski，DJ，Liberski，PP，Kowalczyk，P.，Albrecht，J.，2004]。谷氨酰胺转运蛋白SNAT3的表达增加是恶性神经胶质瘤的标志。 NeuroReport 15，575-578]，但与其他Gln转运蛋白相比，它在肿瘤生长中的作用尚不清楚。胶质细胞瘤原位的深刻的促进生长的作用之一是酸化细胞外空间。在肾脏中，SN1（SNAT3）mRNA参与了对酸中毒的适应。因此，在这项研究中，在酸性介质（AI）（pH 6.5）中孵育了4h的人（T98G）和大鼠（C6）胶质瘤细胞中，测量了编码SN1（SNAT3）和其他Gln转运蛋白的mRNA的表达。 MTT分析显示AI细胞没有细胞丢失，并且通过荧光探针（BCECF-AM）测量的细胞内pH（pHi）在C6和T98G细胞中呈弱碱性，表明该细胞已适应AI。 AI显着降低了C6（降低60％）和T98G细胞（降低50％）中SN1（SNAT3）mRNA的表达。在将C6细胞转移回中性培养基后4h内，这种减少就消失了。在任何一个细胞系中，AI均不影响ASCT2 mRNA（系统ASC），ATA1 mRNA（系统A）和SN2（SNAT5）mRNA（系统N）的表达。在中性培养基中生长的C6或T98G细胞中的[（3）H] Gln摄取主要由系统ASCT2介导：系统N仅占摄取的约7％。 AI不会影响总的Gln摄取，只是稍微降低了系统N介导的摄取成分。因此，SN1（SNAT3）似乎不参与培养的神经胶质瘤细胞适应酸性毫。

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