首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >The ubiquitin-proteasome system in colorectal cancer.
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The ubiquitin-proteasome system in colorectal cancer.

机译:大肠癌中的泛素-蛋白酶体系统。

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摘要

The proteasome is a multiprotein complex that regulates the stability of hundreds of cellular proteins and thus, it is implicated in virtually all cellular functions. Most of the time, to be recognized and processed by the proteasome, a protein has to be linked to a chain of ubiquitin molecules. Cell proliferation, apoptosis, angiogenesis and motility, processes with particular importance for carcinogenesis are regulated by the ubiquitin-proteasome system (UPS). In colorectal epithelium, UPS plays a role in the regulation of the Wnt/beta-catenin/APC/TCF4 signaling which regulates proliferation of colorectal epithelial cells in the bottom of the crypts and the inhibition of this proliferation as cells move towards colon villi tips. In most colorectal cancers APC (Adenomatous Polyposis Coli) disabling mutations interfere with the ability of the proteasome to degrade beta-catenin leading to uninhibited cell proliferation. Other key molecules in colorectal carcinogenesis such as p53, Smad4 and components of the k-ras pathways are also regulated by the UPS. In this review I discuss the role of UPS in colorectal carcinogenesis and colorectal cancer prognosis and aspects of its inhibition for therapeutic purposes.
机译:蛋白酶体是一种多蛋白复合物,可调节数百种细胞蛋白的稳定性,因此实际上涉及所有细胞功能。大多数时候,要被蛋白酶体识别和加工,蛋白质必须与泛素分子链相连。细胞增殖,凋亡,血管生成和运动性,对于癌发生特别重要的过程受泛素-蛋白酶体系统(UPS)调节。在结直肠上皮中,UPS在Wnt /β-catenin/ APC / TCF4信号传导的调节中起作用,该信号调节隐窝底部结直肠上皮细胞的增殖,并在细胞向结肠绒毛尖端移动时抑制这种增殖。在大多数结肠直肠癌中,致残性APC(腺瘤性息肉病)突变会干扰蛋白酶体降解β-catenin的能力,从而导致细胞增殖不受抑制。大肠癌发生中的其他关键分子,例如p53,Smad4和k-ras途径的成分也受UPS的调节。在这篇综述中,我讨论了UPS在结直肠癌发生和结直肠癌预后中的作用以及其在治疗方面的抑制作用。

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