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Blockage of TGF- α Induced by Spherical Silica Nanoparticles Inhibits Epithelial-Mesenchymal Transition and Proliferation of Human Lung Epithelial Cells

Blockage of TGF- α Induced by Spherical Silica Nanoparticles Inhibits Epithelial-Mesenchymal Transition and Proliferation of Human Lung Epithelial Cells

Background. Xuanwei City in Yunnan province has been one of the towns with highest lung cancer mortality in China. The high content of amorphous silica in the bituminous coal from Xuanwei of Yunnan is mainly present as irregular and spherical silica nanoparticles (SiNPs). It has been reported that silica nanoparticles in bituminous coal correlated with the high incidence of lung cancer in Xuanwei. To explore the role and mechanism of SiNPs in the tumorigenesis of lung cancer in Xuanwei, human mononuclear cells (THP-1) and human bronchial epithelial cells (BEAS-2B) were cocultured in a transwell chamber. Combined with Benzo[a]pyrene-7, 8-dihydrodiol-9, and 10-epoxide (BPDE), SiNPs could significantly promote the proliferation and Epithelial-Mesenchymal Transition (EMT) and inhibit apoptosis of BEAS-2B cells and induce the release of TGF-α from THP-1 cells. After neutralizing TGF-α with antibody, the proliferation and EMT were decreased and enhanced apoptosis of BEAS-2B cells. Furthermore, the results showed that TGF-α in the sera of patients with lung adenocarcinoma in Xuanwei were significantly higher than in patients with benign pulmonary lesions in Xuanwei and those with lung adenocarcinoma in outside of Xuanwei of Yunnan. Taken together, our study found that SiNPs promoted the proliferation and EMT of BEAS-2B cells by inducing the release of TGF-α from THP-1 cells.
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YiXun Li, Huan Li, Yong Duan, XueMei Cai, DingYun You, Feng Zhou, ChuanQi Yang, XiaoYu Tuo, ZiJie Liu

  • Biomed Res Int
  • 3.2
  • 2019 Feb 18;2019:8231267.
  • Human
  • 抗体芯片
  • 生物标志物
  • 生物标志物
  • 上皮细胞
  • Adiponectin/Acrp30,IFN-gamma,CCL2/MCP-1,Angiogenin,IGFBP-2,CCL7/MCP-3,Angiopoietin-1,IGFBP-3,M-CSF,Angiopoietin-2,IL-1 alpha/IL-1F1,MIF,Apolipoprotein A1,IL-1 beta/IL-1F2,CXCL9/MIG,BAFF/BLyS/TNFSF13B,IL-1ra/IL-1F3,CCL3/CCL4 MIP-1 alpha/beta,BDNF,IL-2,CCL20/MIP-3 alpha,CD14,IL-3,CCL19/MIP-3 beta,CD30,IL-4,MMP-9,CD31/PECAM-1,IL-5,Myeloperoxidase,CD40 Ligand/TNFSF5,IL-6,Osteopontin (OPN),Chitinase 3-like,IL-8,PDGF-AA,Complement Component C5/C5a,IL-10,PDGF-AB/BB,Complement Factor D,IL-11,Pentraxin 3/TSF-14,C-Reactive Protein/CRP,IL-12 p70,CXCL4/PF4,Cripto-1,IL-13,RAGE,Cystatin C,IL-15,CCL5/RANTES,Dkk-1,IL-16,RBP4,DPPIV/CD26,IL-17A,Relaxin-2,EGF,IL-18 BPa,Resistin,CXCL5/ENA-78,IL-19,CXCL12/SDF-1 alpha,Endoglin/CD105,IL-22,Serpin E1/PAI-1,EMMPRIN,IL-23,SHBG,Fas Ligand,IL-24,ST2/IL1 R4,FGF basic,IL-27,CCL17/TARC,KGF/FGF-7,IL-31,TFF3,FGF-19,IL-32 alpha/beta/gamma,TfR,Flt-3 Ligand,IL-33,TGF-alpha,G-CSF,IL-34,Thrombospondin-1,GDF-15,CXCL10/IP-10,TIM-1,GM-CSF,CXCL11/I-TAC,TNF-alpha,CXCL1/GRO alpha,Kallikrein 3/PSA,uPAR,Growth Hormone (GH),Leptin,VCAM-1,HGF,LIF,VEGF,ICAM-1/CD54,Lipocalin-2/NGAL,Vitamin D BP
  • doi: 10.1155/2019/8231267.

相关货号

LXAH105-1

Abstract

Background. Xuanwei City in Yunnan province has been one of the towns with highest lung cancer mortality in China. The high content of amorphous silica in the bituminous coal from Xuanwei of Yunnan is mainly present as irregular and spherical silica nanoparticles (SiNPs). It has been reported that silica nanoparticles in bituminous coal correlated with the high incidence of lung cancer in Xuanwei. To explore the role and mechanism of SiNPs in the tumorigenesis of lung cancer in Xuanwei, human mononuclear cells (THP-1) and human bronchial epithelial cells (BEAS-2B) were cocultured in a transwell chamber. Combined with Benzo[a]pyrene-7, 8-dihydrodiol-9, and 10-epoxide (BPDE), SiNPs could significantly promote the proliferation and Epithelial-Mesenchymal Transition (EMT) and inhibit apoptosis of BEAS-2B cells and induce the release of TGF-α from THP-1 cells. After neutralizing TGF-α with antibody, the proliferation and EMT were decreased and enhanced apoptosis of BEAS-2B cells. Furthermore, the results showed that TGF-α in the sera of patients with lung adenocarcinoma in Xuanwei were significantly higher than in patients with benign pulmonary lesions in Xuanwei and those with lung adenocarcinoma in outside of Xuanwei of Yunnan. Taken together, our study found that SiNPs promoted the proliferation and EMT of BEAS-2B cells by inducing the release of TGF-α from THP-1 cells.
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