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首页> 外文期刊>Life sciences >Effects of transforming growth factor #beta#_1 on cell growth and parathyroid hormone-related protein in walker 256 tumor cells
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Effects of transforming growth factor #beta#_1 on cell growth and parathyroid hormone-related protein in walker 256 tumor cells

机译：转化生长因子＃beta＃_1对Walker 256肿瘤细胞生长和甲状旁腺激素相关蛋白的影响

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Hypercalcemic strains of the rat Walker 256 (W256) tumor synthesize parathyroid hormone-related protein (PTHrP) and at least one of them produces an ill-defined transforming growth factor activity. We tested the production of transforming growth factor (TGF) #beta# by a hypercalcemic W256 tumor strain, and assessed its effects on tumor cell growth and PTHrP expression. We found that addition of TGF #beta#_1 for 7 days inhibited cell growth ([~3H)thymidine incorporation and cell number) dose dependently, between 0.04-20 pM. The antiproliferative effect of TGF #beta#_1 on W256 tumor cell growth was likely mediated by binding to high affinity receptors (K_d = 14 pM) in these cells. At different tumor cell growth stages, acidified cell-conditioned medium contained immunoreactive TGF #beta#_1. However, the nonacidified tumor cell-conditioned medium was found to contain neither immunoreactive nor bioactive TGF #beta#. Moreover, exposure of W256 tumor cells to a neutralizing anti-TGF #beta#_1 antibody failed to affect tumor cell proliferation. Thus, W256 tumor cells appear to secrete TGF #beta# in an inactive form. Using reverse transcription followed by PCR, we found that addition of 20 pM TGF #beta#_1 increased its own mRNA expression, apparently by stimulating gene transcription, within 6-12 h in W256 tumor cells. In addition, 20 pM TGF #beta#_1 stimulated PTHrP mRNA in these cells at 24 h; an effect which was mediated, at least in part, by increasing PTHrP mRNA stability. Immunoreactive PTHrP decreased in the W256 tumor cell-conditioned medium after treatment with 20 pM TGF #beta#_1 for 24-48 h. These results support the validity of this W256 tumor strain for in vivo studies to clarify the relative role of TGF #beta#and PTHrP in the pathogenesis of humoral hypercalcemia of malignancy.
机译：大鼠Walker 256（W256）肿瘤的高钙血症毒株会合成甲状旁腺激素相关蛋白（PTHrP），其中至少一种会产生不确定的转化生长因子活性。我们测试了由高钙血症W256肿瘤菌株产生的转化生长因子（TGF）＃beta＃的产生，并评估了其对肿瘤细胞生长和PTHrP表达的影响。我们发现添加TGF＃beta＃_1 7天可剂量依赖性地抑制细胞生长（[〜3H]胸苷掺入和细胞数），介于0.04-20 pM之间。 TGF＃beta＃_1对W256肿瘤细胞生长的抗增殖作用可能是通过与这些细胞中的高亲和力受体（K_d = 14 pM）结合而介导的。在不同的肿瘤细胞生长阶段，酸化的细胞条件培养基含有免疫反应性TGF＃beta＃_1。然而，发现非酸化的肿瘤细胞条件培养基既不包含免疫反应性也不具有生物活性的TGF＃β＃。而且，将W256肿瘤细胞暴露于中和性抗TGF＃β＃_1抗体不能影响肿瘤细胞增殖。因此，W256肿瘤细胞似乎以非活性形式分泌TGF＃beta＃。使用逆转录随后进行PCR，我们发现在W256肿瘤细胞中添加20 pM TGF＃beta＃_1显然是通过刺激基因转录来增加其自身的mRNA表达，这显然是通过刺激基因转录。此外，在第24小时，有20 pM TGF＃beta＃_1刺激了这些细胞中的PTHrP mRNA。这种作用至少部分是通过增加PTHrP mRNA的稳定性来介导的。用20 pM TGF＃beta＃_1处理24-48小时后，在W256肿瘤细胞条件培养基中免疫反应性PTHrP降低。这些结果支持了该W256肿瘤菌株在体内研究中的有效性，以阐明TGF＃beta＃和PTHrP在恶性体液性高钙血症发病机理中的相对作用。

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