Spherical silica nanoparticles promote malignant transformation of BEAS-2B cells by stromal cell-derived factor-1a (SDF-1a)
Spherical silica nanoparticles promote malignant transformation of BEAS-2B cells by stromal cell-derived factor-1a (SDF-1a)
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球形二氧化硅纳米颗粒通过基质细胞衍生因子 1a (SDF-1a) 促进 BEAS-2B 细胞恶性转化
DOI：
10.1177/0300060518814333
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发表时间：
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影响因子：
1.6
通讯作者：
Zi-Jie Liu
中科院分区：
文献类型：
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作者：
Chong Guo;Ding-Yun You;Huan Li;Xiao-Yu Tuo;Zi-Jie Liu
目的：探讨球形二氧化硅纳米颗粒(SiNPs)对人支气管上皮细胞(BEAS-2B)炎症反应的影响。方法：人单核细胞(THP-1)与人BEAS-2B细胞在Transwell小室中共培养，分别加入800 mmol/L苯并[a]芘-7，8-二氢二醇-9，10-环氧化物(BPDE)和12.5 mg/mLSiNPs作用24小时。对于对照组，细胞仅用BPDE处理。测定BEAS-2B细胞的皮下致瘤性和上皮-间充质转化(EMT)。这些细胞被基质细胞衍生因子-1a(SDF-1a)特异性抗体阻断。将800 mmol/L BPDE和12.5 mg/mLSiNPs处理的细胞与对照细胞和体内移植瘤进行EMT分析。检测23例宣威肺腺癌、25例宣威外肺腺癌和22例宣威肺良性病变患者血清SDF-1a水平。结果：SiNPs显著促进BEAS-2B细胞的生长和EMT，诱导SDF-1a释放，激活AKT(Ser473)。SDF-1a抗体阻断后，BEAS-2B细胞的EMT、磷酸化AKT(Ser473)和糖原合成酶激酶-3b水平均降低。结论：SiNPs联合BPDE通过诱导THP-1细胞释放SDF-1a，通过AKT途径促进BEAS-2B细胞的EMT。
Objective: This study aimed to examine the role of spherical silica nanoparticles (SiNPs) on human bronchial epithelial (BEAS-2B) cells through inflammation..Methods: Human mononuclear (THP-1) cells and BEAS-2B cells were co-cultured in transwell chambers and treated with 800 mmol/L benzo[a]pyrene-7, 8-dihydrodiol-9, 10-epoxide (BPDE) and 12.5 mg/mL SiNPs for 24 hours. For controls, cells were treated with BPDE alone. Subcutaneous tumorigenicity and epithelial-mesenchymal transition (EMT) of BEAS-2B cells were measured. The cells were blocked with a stromal cell-derived factor-1a (SDF-1a)-specific antibody. EMTwas analyzed in cells treated with 800mmol/L BPDE and 12.5 mg/mL SiNPs relative to matched control cells and xenografts in vivo. Serum SDF-1a levels were measured in 23 patients with lung adenocarcinoma in Xuanwei, in 25 with lung adenocarcinoma outside Xuanwei, and in 22 with benign pulmonary lesions in Xuanwei..Results: SiNPs significantly promoted tumorigenesis and EMT, induced the release of SDF-1a, and activated AKT (ser473) in BEAS-2B cells. EMT and phosphorylated AKT (ser473) and glycogen synthase kinase-3b levels were decreased when blocked by SDF-1a antibody in BEAS-2B.cells. SDF-1a was mainly secreted by THP-1 cells..Conclusion: SiNPs combined with BPDE promote EMT of BEAS-2B cells via the AKT pathway by inducing release of SDF-1a from THP-1 cells.