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赖氨酰氧化酶与口腔鳞状细胞癌中细胞增殖和血管生成的增强。

Lysyl oxidase and enhancement of cell proliferation and angiogenesis in oral squamous cell carcinoma.

机构信息

Institute of Oral Biology, School of Dentistry, National Yang-Ming University, Taipei, Taiwan.

出版信息

Head Neck. 2013 Feb;35(2):250-6. doi: 10.1002/hed.22959. Epub 2012 Feb 24.

DOI:10.1002/hed.22959
PMID:22367676
Abstract

BACKGROUND

Lysyl oxidase (LOX) is a copper-dependent enzyme that cross-links collagen and elastin in the extracellular matrix. LOX overexpressed in various tumors. The manner in which LOX affects tumor growth remains controversial.

METHODS

Chemical treatment and gene transfection were used to induce LOX overexpression or inhibition in cell lines SAS and SVEC4-10. LOX mRNA, protein, and activity were confirmed before tube formation assay and tumorigenesis. The microvessels in the tumor section were detected by immunostaining CD31-positive endothelial cells.

RESULTS

LOX overexpression and copper induction of LOX activity increased SVEC4-10 tube formation. LOX silencing and β-aminopropionitrile inhibition of LOX activity had opposite effects. LOX overexpression increased proliferation and proliferating cell nuclear antigen expression. High LOX expression clones increased tumor size in a tumorigenesis model. The microvascular numbers were higher in LOX overexpression tumors than in control tumors.

CONCLUSION

LOX can induce cell proliferation and angiogenesis in oral squamous cell carcinoma.

摘要

背景

赖氨酰氧化酶(LOX)是一种依赖铜的酶,可在细胞外基质中交联胶原蛋白和弹性蛋白。LOX 在各种肿瘤中过度表达。LOX 影响肿瘤生长的方式仍存在争议。

方法

化学处理和基因转染用于诱导 SAS 和 SVEC4-10 细胞系中的 LOX 过表达或抑制。在管形成测定和致瘤之前,确认 LOX mRNA、蛋白质和活性。通过免疫染色 CD31 阳性内皮细胞检测肿瘤切片中的微血管。

结果

LOX 过表达和铜诱导 LOX 活性增加了 SVEC4-10 管形成。LOX 沉默和β-氨基丙腈抑制 LOX 活性则产生相反的效果。LOX 过表达增加了增殖和增殖细胞核抗原的表达。在致瘤模型中,高 LOX 表达克隆增加了肿瘤大小。LOX 过表达肿瘤中的微血管数量高于对照肿瘤。

结论

LOX 可诱导口腔鳞状细胞癌中的细胞增殖和血管生成。

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