首页> 外文会议>Biomedical Engineering and Biotechnology (iCBEB), 2012 International Conference on >The Biological Effects and Mechanisms of Foxp3 in Lewis Lung Cancer Cell
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The Biological Effects and Mechanisms of Foxp3 in Lewis Lung Cancer Cell

机译:Foxp3在Lewis肺癌细胞中的生物学效应及其机制。

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Forkhead box P3 (Foxp3) has been considered to be the key regulator for the development and function of CD4+CD25+ Treg cells(regulatory T cells, Tregs). The high levels of Tregs in peripheral blood and tumor tissues have been reported in cancer patients and have been closely related to worse prognosis. Recent reports showed the expression of Foxp3 were not only in Tregs, but also in tumor cells. Foxp3 expression in lung cancer cells and its functions have not been reported now. We constructed the recombinant plasmid pcDNA3.1-Foxp3 and transiently transfected mouse lewis lung carcinoma (LLC) cells to investigate the biological effects and mechanisms of Foxp3 by detecting cells proliferation, cell apoptosis and cell cycle. The results illuminated that Foxp3 protein were highly expressed in Foxp3 transfected LLC cells. Foxp3 expression in LLC significantly inhibited cell proliferation. The related mechanism for Foxp3 inhibiting cell proliferation has no relationship with cell apoptosis, but has relationship with cell cycle. Foxp3 transfected LLC cells were arrested in the G0-G1 phase. In conclusion, Foxp3 in LLC inhibited cell proliferation and cell blocking in the G0-G1 phase might be its main mechanism.
机译:叉头盒P3(Foxp3)被认为是CD4 + CD25 + Treg细胞(调节性T细胞,Tregs)的发育和功能的关键调节剂。在癌症患者中已经报道了外周血和肿瘤组织中高水平的Tregs,并且与不良预后密切相关。最近的报道表明Foxp3的表达不仅在Treg中,而且在肿瘤细胞中也表达。 Foxp3在肺癌细胞中的表达及其功能目前尚无报道。我们构建了重组质粒pcDNA3.1-Foxp3,并瞬时转染了小鼠刘易斯肺癌(LLC)细胞,通过检测细胞增殖,细胞凋亡和细胞周期来研究Foxp3的生物学效应和机制。结果表明Foxp3蛋白在Foxp3转染的LLC细胞中高表达。 LLC中的Foxp3表达明显抑制细胞增殖。 Foxp3抑制细胞增殖的相关机制与细胞凋亡无关,但与细胞周期有关。 Foxp3转染的LLC细胞被阻滞在G0-G1期。总之,LLC中的Foxp3抑制了细胞增殖,G0-G1期的细胞阻滞可能是其主要机制。

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