Store-operated Ca2+ entry does not control proliferation in primary cultures of human metastatic renal cellular carcinoma.
Store-operated Ca2+ entry does not control proliferation in primary cultures of human metastatic renal cellular carcinoma.
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DOI：
10.1155/2014/739494
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发表时间：
2014
影响因子：
--
通讯作者：
Moccia F
中科院分区：
文献类型：
--
作者：
Dragoni S;Turin I;Laforenza U;Potenza DM;Bottino C;Glasnov TN;Prestia M;Ferulli F;Saitta A;Mosca A;Guerra G;Rosti V;Luinetti O;Ganini C;Porta C;Pedrazzoli P;Tanzi F;Montagna D;Moccia F
储存操作的Ca2+进入（SOCE）在肌醇-1,4,5-三磷酸（InsP3）敏感的Ca2+池耗尽后被激活，以调节从原发性或转移性病变建立的永活细胞系的增殖。SOCE的分子性质可能涉及内质网（ER） Ca2+库中感知Ca2+水平的Stim1和质膜上的许多Ca2+可渗透通道，包括Orai1、Orai3和典型瞬时受体（TRPC1-7）离子通道家族的成员。本研究旨在评估从重度预处理的转移性肾细胞癌（mRCC）患者继发病变中分离的原代培养物中是否表达SOCE并控制其增殖。SOCE是在ER Ca2+储存的药理学耗尽后诱导的，但不是由insp3依赖性Ca2+释放引起的。转移性RCC细胞表达Stim1-2、Orai1-3和TRPC1-7转录物和蛋白。在这些细胞中，SOCE对BTP-2、10µM Gd3+和Pyr6不敏感，而对100µM Gd3+、2-APB和羧基氨基三唑（CAI）有抑制作用。Gd3+、2-APB和CAI均未损伤mRCC细胞的增殖。一致地，没有检测到Ca2+信号是由生长因子刺激引起的。因此，表达功能性SOCE，但不控制从多激酶抑制剂耐药患者分离的mRCC细胞的增殖。
Store-operated Ca2+ entry (SOCE) is activated following depletion of the inositol-1,4,5-trisphosphate (InsP3)-sensitive Ca2+ pool to regulate proliferation in immortalized cell lines established from either primary or metastatic lesions. The molecular nature of SOCE may involve both Stim1, which senses Ca2+ levels within the endoplasmic reticulum (ER) Ca2+ reservoir, and a number of a Ca2+-permeable channels on the plasma membrane, including Orai1, Orai3, and members of the canonical transient receptor (TRPC1–7) family of ion channels. The present study was undertaken to assess whether SOCE is expressed and controls proliferation in primary cultures isolated from secondary lesions of heavily pretreated metastatic renal cell carcinoma (mRCC) patients. SOCE was induced following pharmacological depletion of the ER Ca2+ store, but not by InsP3-dependent Ca2+ release. Metastatic RCC cells express Stim1-2, Orai1–3, and TRPC1–7 transcripts and proteins. In these cells, SOCE was insensitive to BTP-2, 10 µM Gd3+ and Pyr6, while it was inhibited by 100 µM Gd3+, 2-APB, and carboxyamidotriazole (CAI). Neither Gd3+ nor 2-APB or CAI impaired mRCC cell proliferation. Consistently, no detectable Ca2+ signal was elicited by growth factor stimulation. Therefore, a functional SOCE is expressed but does not control proliferation of mRCC cells isolated from patients resistant to multikinase inhibitors.
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影响因子：
5.6
作者：
Bomben, Valerie C.;Turner, Kathryn L.;Barclay, Tia-Tabitha C.;Sontheimer, Harald
通讯作者：
Sontheimer, Harald
影响因子：
4
作者：
Enfissi, A;Prigent, S;Capiod, T
通讯作者：
Capiod, T
影响因子：
11.2
作者：
Kang SS;Han KS;Ku BM;Lee YK;Hong J;Shin HY;Almonte AG;Woo DH;Brat DJ;Hwang EM;Yoo SH;Chung CK;Park SH;Paek SH;Roh EJ;Lee SJ;Park JY;Traynelis SF;Lee CJ
通讯作者：
Lee CJ
影响因子：
2.8
作者：
Harteneck C;Gollasch M
通讯作者：
Gollasch M
影响因子：
4.3
作者：
Flanigan, Robert C;Campbell, Steven C;Picken, Maria M
通讯作者：
Picken, Maria M