首页> 美国卫生研究院文献>Journal of Veterinary Science >Downregulation of cellular prion protein inhibited the proliferation and invasion and induced apoptosis of Mareks disease virus-transformed avian T cells
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Downregulation of cellular prion protein inhibited the proliferation and invasion and induced apoptosis of Mareks disease virus-transformed avian T cells

机译:细胞病毒蛋白的下调抑制了马立克氏病病毒转化的禽T细胞的增殖和侵袭并诱导了细胞凋亡

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摘要

Cellular prion protein (PrPC) is ubiquitously expressed in the cytomembrane of a considerable number of eukaryotic cells. Although several studies have investigated the functions of PrPC in cell proliferation, cell apoptosis, and tumorigenesis of mammals, the correlated functions of chicken PrPC (chPrPC) remain unknown. In this study, stable chPrPC-downregulated Marek's disease (MD) virus-transformed avian T cells (MSB1-SiRNA-3) were established by introducing short interfering RNA (SiRNA) targeting chicken prion protein genes. We found that downregulation of chPrPC inhibits proliferation, invasion, and migration, and induces G1 cell cycle phase arrest and apoptosis of MSB1-SiRNA-3 cells compared with Marek's disease virus-transformed avian T cells (MSB1) and negative control cells. To the best of our knowledge, the present study provides the first evidence supporting the positive correlation between the expression level of chPrPC and the proliferation, migration, and invasion ability of MSB1 cells, but appears to protect MSB1 cells from apoptosis, which suggests it functions in the formation and development of MD tumors. This evidence may contribute to future research into the specific molecular mechanisms of chPrPC in the formation and development of MD tumors.
机译:细胞pr病毒蛋白(PrP C )在大量真核细胞的细胞膜中普遍表达。尽管有几项研究调查了PrP C 在哺乳动物细胞增殖,细胞凋亡和肿瘤发生中的功能,但鸡PrP C (chPrP C < / sup>)仍然未知。在这项研究中,通过引入靶向鸡病毒蛋白基因的短干扰RNA(SiRNA),建立了稳定的chPrP C 下调的马立克氏病(MD)病毒转化的禽T细胞(MSB1-SiRNA-3)。我们发现,与马立克氏病病毒转化的禽类T细胞(MSB1)相比,chPrP C 的下调抑制了MSB1-SiRNA-3细胞的增殖,侵袭和迁移,并诱导了G1细胞周期的阻滞和凋亡。 )和阴性对照细胞。据我们所知,本研究提供了第一个证据,证明chPrP C 的表达水平与MSB1细胞的增殖,迁移和侵袭能力呈正相关,但似乎可以保护MSB1。细胞凋亡,提示它在MD肿瘤的形成和发展中起作用。这一证据可能有助于进一步研究chPrP C 在MD肿瘤形成和发展中的具体分子机制。

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