Release of collagen type IV degrading activity from C6 astrocytoma cells and cell density.

Release of collagen type IV degrading activity from C6 astrocytoma cells and cell density.
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C6 星形细胞瘤细胞和细胞密度中释放 IV 型胶原蛋白降解活性。

DOI:
10.3171/jns.1996.84.6.1013
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发表时间:
1996
影响因子:
4.1
通讯作者:
R. Del Maestro
R. Del Maestro
中科院分区:
医学1区
文献类型:
--
作者:
M. Tamaki;W. McDonald;R. Del Maestro

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IV型胶原是血管基底膜的主要蛋白质成分,其降解是启动肿瘤相关血管生成的关键。作者研究了细胞密度对单层培养的C6星形细胞瘤细胞释放IV型胶原降解活性的影响。通过生化、免疫细胞化学和Western印迹分析评价IV型胶原降解活性的释放。结果表明,增加平板密度和增加细胞密度与每个肿瘤细胞释放的IV型胶原降解活性降低有关。这些发现表明存在依赖于细胞间通讯的调节机制,该机制调节IV型胶原降解活性的释放。将这些结果外推到体内肿瘤微环境将表明,远离主要肿瘤块的单个和/或小群侵袭性肿瘤细胞将释放大量的IV型胶原降解活性,这可能是它们继续侵袭和血管生成的关键。
Type IV collagen is a major protein component of the vascular basement membrane and its degradation is crucial to the initiation of tumor-associated angiogenesis. The authors have investigated the influence of cell density on the release of collagen type IV degrading activity by C6 astrocytoma cells in monolayer culture. The release of collagen type IV degrading activity was assessed biochemically, immunocytochemically, and by Western blot analysis. The results demonstrate that increasing plating density and increasing cell density are associated with decreased collagen type IV degrading activity released per tumor cell. These findings indicate the existence of regulatory mechanisms dependent on cell-cell communication, which modulate release of collagen type IV degrading activity. The extrapolation of these results to the in vivo tumor microenvironment would suggest that individual and/or small groups of invading tumor cells, distant from the main tumor mass, would release substantial collagen type IV degrading activity, which may be crucial to their continued invasion and to angiogenesis.
DOI: 10.1016/s0021-9258(18)71503-2
发表时间: 1989-10
期刊: The Journal of biological chemistry
影响因子: --
作者:
W. Stetler-Stevenson;H. Krutzsch;L. Liotta
通讯作者: W. Stetler-Stevenson;H. Krutzsch;L. Liotta
A431 人表皮样癌细胞培养物中 92-kd IV 型胶原酶活性的密度依赖性诱导。
DOI: --
发表时间: 1994
期刊: The American journal of pathology
影响因子: --
作者:
Xie,B;Bucana,CD;Fidler,IJ
通讯作者: Fidler,IJ