Orend Gertraud
Institute of Biochemistry and Genetics, Departement fiir Klinisch Biologische Wissenschaften (DKBW), Center for Biomedicine, University Basel, Mattenstrasse 28, CH-4058 Basel, Switzerland.
Int J Biochem Cell Biol. 2005 May;37(5):1066-83. doi: 10.1016/j.biocel.2004.12.002. Epub 2005 Jan 18.
The prominent expression of tenascin-C in the stroma of most solid tumors, first observed in the mid 1980s, implicates tenascin-C in tumorigenesis. This is also supported by in vitro experiments that demonstrate the capacity of tenascin-C to stimulate tumor growth by various mechanisms including promotion of proliferation, escaping immuno-surveillance and positively influencing angiogenesis. However, tumorigenesis in tenascin-C knock-out mice is not significantly different from that observed in control animals. Perhaps this is not unexpected if one considers that tenascin-C may act as an oncogene. The potential role of tenascin-C in tumorigenesis through its oncogenic action on cellular signaling will be discussed in this review, including how tenascin-C mediated tumor cell detachment might affect genome stability.
20世纪80年代中期首次观察到,大多数实体瘤基质中肌腱蛋白-C的显著表达表明其与肿瘤发生有关。体外实验也支持这一点,这些实验证明肌腱蛋白-C能够通过多种机制刺激肿瘤生长,包括促进增殖、逃避免疫监视以及对血管生成产生积极影响。然而,肌腱蛋白-C基因敲除小鼠的肿瘤发生与对照动物中观察到的情况并无显著差异。如果认为肌腱蛋白-C可能作为一种癌基因,那么这或许并不意外。本综述将讨论肌腱蛋白-C通过其对细胞信号传导的致癌作用在肿瘤发生中的潜在作用,包括肌腱蛋白-C介导的肿瘤细胞脱离如何影响基因组稳定性。