ERK, Extracellular signal-related kinase

  • 文章类型: Journal Article
    肺癌是全球癌症相关死亡的主要原因,最常见的肺癌亚型是腺癌。RhoQ是Rho家族GTP酶,具有与Cdc42和RhoJ的一级序列和结构相似性。RhoQ通过膜运输参与神经突生长,并且对于成熟脂肪细胞中胰岛素刺激的葡萄糖摄取至关重要。然而,RhoQ在肺腺癌(LUAD)中的作用尚不清楚.在这项研究中,将RhoQsiRNA引入A549和PC-9细胞中。采用Westernblot和transwell法检测EMT相关基因的表达水平和侵袭能力。探讨RhoQ表达与LUAD预后的关系,使用Kaplan-Meier绘图仪。我们发现抑制RhoQ表达可促进TGF-β介导的EMT和LUAD细胞系的侵袭。此外,RhoQ敲低增加Smad3磷酸化和蜗牛表达,表明RhoQ在EMT过程中参与TGF/Smad信号传导。此外,Kaplan-Meier绘图仪分析显示,低RhoQ水平与LUAD患者总体生存率低相关。总之,这些发现揭示了RhoQ在LUAD中作为TGF-β介导的EMT的负调节因子的作用。
    Lung cancer is the leading cause of cancer-related deaths worldwide, and the most common subtype of lung cancer is adenocarcinoma. RhoQ is a Rho family GTPase with primary sequence and structural similarities to Cdc42 and RhoJ. RhoQ is involved in neurite outgrowth via membrane trafficking and is essential for insulin-stimulated glucose uptake in mature adipocytes. However, the function of RhoQ in lung adenocarcinoma (LUAD) remains unclear. In this study, RhoQ siRNAs were introduced into A549 and PC-9 cells. Expression level of EMT-related genes and invasion ability were investigated using Western blot and transwell assay. To examine the relationship between RhoQ expression and prognosis of LUAD, Kaplan-Meier plotter was used. We discovered that suppressing RhoQ expression promoted TGF-β-mediated EMT and invasion in LUAD cell lines. Furthermore, RhoQ knockdown increased Smad3 phosphorylation and Snail expression, indicating that RhoQ was involved in TGF/Smad signaling during the EMT process. Moreover, Kaplan-Meier plotter analysis revealed that low RhoQ levels were associated with poor overall survival in patients with LUAD. In conclusion, these findings shed light on RhoQ\'s role as a negative regulator of TGF-β-mediated EMT in LUAD.
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  • 文章类型: Journal Article
    某些食物成分具有免疫调节作用。这项研究的目的是阐明甘蓝型油菜的免疫刺激活性的机制。我们证明了口服B.rapaL.的不溶性部分的小鼠的自然杀伤(NK)活性和干扰素(IFN)-γ产生的增强。和NK1.1+细胞是负责产生IFN-γ的主要细胞。此外,结果表明,不溶性部分中的活性化合物被树突状细胞上的Toll样受体(TLR)2,TLR4和C型凝集素受体识别,它们激活了信号级联,如MAPK,NF-κB,还有Syk.这些发现表明,B.rapaL.是一种潜在的有前途的免疫改善材料,它可能有助于通过激活先天免疫来预防免疫疾病,如感染和癌症。
    Certain food components possess immunomodulatory effects. The aim of this study was to elucidate the mechanism of the immunostimulatory activity of Brassica rapa L. We demonstrated an enhancement of natural killer (NK) activity and interferon (IFN)-γ production in mice that were orally administered an insoluble fraction of B. rapa L. The insoluble fraction of B. rapa L. significantly induced IFN-γ production in mouse spleen cells in an interleukin (IL)-12-dependent manner, and NK1.1+ cells were the main cells responsible for producing IFN-γ. Additionally, the results suggested that the active compounds in the insoluble fraction were recognized by Toll-like receptor (TLR) 2, TLR4, and C-type lectin receptors on dendritic cells, and they activated signaling cascades such as MAPK, NF-κB, and Syk. These findings suggest that B. rapa L. is a potentially promising immuno-improving material, and it might be useful for preventing immunological disorders such as infections and cancers by activating innate immunity.
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  • 文章类型: Journal Article
    The bone morphogenetic proteins, (BMP)s are regulatory peptides that have significant effects on the growth and differentiation of gastrointestinal tissues. In addition, the BMPs have been shown to exert anti-inflammatory actions in the gut and to negatively regulate the growth of gastric neoplasms. The role of BMP signaling in the regulation of gastric metaplasia, dysplasia and neoplasia has been poorly characterized. Transgenic expression in the mouse stomach of the BMP inhibitor noggin leads to decreased parietal cell number, increased epithelial cell proliferation, and to the emergence of SPEM. Moreover, expression of noggin increases Helicobacter-induced inflammation and epithelial cell proliferation, accelerates the development of dysplasia, and it increases the expression of signal transducer and activator of transcription 3 (STAT3) and of activation-induced cytidine deaminase (AID). These findings provide new clues for a better understanding of the pathophysiological mechanisms that regulate gastric inflammation and the development of both dysplastic and neoplastic lesions of the stomach.
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