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首页> 外文期刊>Oncology letters >Antimicrobial peptide LL-37 promotes the proliferation and invasion of skin squamous cell carcinoma by upregulating DNA-binding protein A
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Antimicrobial peptide LL-37 promotes the proliferation and invasion of skin squamous cell carcinoma by upregulating DNA-binding protein A

机译:抗菌肽LL-37通过上调DNA结合蛋白A促进皮肤鳞状细胞癌的增殖和侵袭

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The antimicrobial peptide LL-37 not only contributes to the host defence against microbial invasion but also regulates immune activity, angiogenesis and cell proliferation. Studies have shown that LL-37 participates in the development of a variety of tumours, such as lung cancer, ovarian cancer, breast cancer and melanoma. However, the role of LL-37 in the development of skin squamous cell carcinoma (SCC) is not clear. The present study used immunohistochemistry to confirm that the expression of human DNA-binding protein A (dbpA) was increased in SCC tissues. After stimulating SCC A341 cells, LL-37 was shown promote the proliferation, migration and invasion of these malignant cells. LL-37 also promoted the upregulation of dbpA mRNA and protein expression. In addition, after using small interfering RNA to silence the normal dbpA expression in these malignant cells, the proliferation and invasion of the tumor cells were significantly reduced. When the NF-.B inhibitor PDTC was used to inhibit the process of LL-37-stimulated cells, it was found that the original upregulated expression of dbpA was downregulated. Overall, the present demonstrated that by upregulating the expression of dbpA, LL-37 can promote the proliferation and invasion of tumour cells, and that this process depends on the NF-kappa B signalling pathway.
机译:抗菌肽LL-37不仅有助于宿主防御微生物入侵,而且还调节免疫活性,血管生成和细胞增殖。研究表明,LL-37参与多种肿瘤的发展,例如肺癌,卵巢癌,乳腺癌和黑色素瘤。但是,LL-37在皮肤鳞状细胞癌(SCC)发生中的作用尚不清楚。本研究使用免疫组织化学来证实人类DNA结合蛋白A(dbpA)的表达在SCC组织中增加。刺激SCC A341细胞后,显示LL-37可促进这些恶性细胞的增殖,迁移和侵袭。 LL-37还促进dbpA mRNA和蛋白表达的上调。另外,在使用小的干扰RNA使这些恶性细胞中的正常dbpA表达沉默之后,肿瘤细胞的增殖和侵袭显着降低。当使用NF-.B抑制剂PDTC抑制LL-37刺激的细胞过程时,发现dbpA的原始上调表达被下调。总体而言,本发明证明通过上调dbpA的表达,LL-37可以促进肿瘤细胞的增殖和侵袭,并且该过程取决于NF-κB信号传导途径。

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