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源自已建立的人类恶性胶质瘤细胞系的TM-1细胞产生血小板衍生生长因子(PDGF)、转化生长因子-α(TGF-α)和转化生长因子-β(TGF-β),它们协同发挥自分泌生长促进的刺激作用。

TM-1 cells from an established human malignant glioma cell line produce PDGF, TGF-alpha, and TGF-beta which cooperatively play a stimulatory role for an autocrine growth promotion.

作者信息

Kurimoto M, Endo S, Arai K, Horie Y, Nogami K, Takaku A

机构信息

Department of Neurosurgery, Toyama Medical and Pharmaceutical University, Faculty of Medicine, Japan.

出版信息

J Neurooncol. 1994;22(1):33-44. doi: 10.1007/BF01058353.

Abstract

We have previously established a human malignant glioma cell line, TM-1. TM-1 cells could proliferate in the serum-free medium. In the present study, immunochemical analysis demonstrated that platelet-derived growth factor (PDGF), transforming growth factor (TGF)-alpha, and TGF-beta are present in the serum-free medium conditioned by growing TM-1 cells. While the cells appeared to possess a single type of binding sites for epidermal growth factor (EGF) with properties comparable to those determined for other tumor cells, the conditioned medium did not contain EGF.PDGF, TGF-alpha, and EGF added exogenously to serum-free media stimulated thymidine incorporation into DNA of TM-1 cells. In addition, antibodies specific for PDGF and TGF-alpha suppressed this activity. These results indicate autocrine and stimulatory roles of PDGF and TGF-alpha for the proliferation of TM-1 cells. As observed for other tumor cells, TGF-beta by itself weakly suppressed thymidine incorporation by TM-1 cells. However, TGF-beta employed in combination with TGF-alpha or EGF appeared to stimulate thymidine incorporation, suggesting that a cooperative action of TGF-beta with different growth factors may be involved in the stimulatory growth regulation at least for TM-1 cells.

摘要

我们之前建立了一种人类恶性胶质瘤细胞系TM-1。TM-1细胞能够在无血清培养基中增殖。在本研究中,免疫化学分析表明,血小板衍生生长因子(PDGF)、转化生长因子(TGF)-α和TGF-β存在于由生长的TM-1细胞条件培养的无血清培养基中。虽然这些细胞似乎具有一种与其他肿瘤细胞所确定的性质相当的表皮生长因子(EGF)结合位点类型,但条件培养基中不含EGF。向无血清培养基中外源添加的PDGF、TGF-α和EGF刺激了胸腺嘧啶核苷掺入TM-1细胞的DNA中。此外,针对PDGF和TGF-α的特异性抗体抑制了这种活性。这些结果表明PDGF和TGF-α对TM-1细胞增殖具有自分泌和刺激作用。正如在其他肿瘤细胞中观察到的那样,TGF-β本身对TM-1细胞胸腺嘧啶核苷掺入的抑制作用较弱。然而,TGF-β与TGF-α或EGF联合使用似乎刺激了胸腺嘧啶核苷掺入,这表明TGF-β与不同生长因子的协同作用可能至少参与了TM-1细胞的刺激生长调节。

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