The Potential Role of Cathepsin K in Non-Small Cell Lung Cancer.
The Potential Role of Cathepsin K in Non-Small Cell Lung Cancer.
复制标题
组织蛋白酶 K 在非小细胞肺癌中的潜在作用
DOI：
10.3390/molecules25184136
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发表时间：
2020-09-10
期刊：
影响因子：
--
通讯作者：
Zhong L
中科院分区：
文献类型：
--
作者：
Yang H;Heyer J;Zhao H;Liang S;Guo R;Zhong L
(1)背景：组织蛋白酶K在多种恶性肿瘤中过度表达。然而，关于组织蛋白酶K参与非小细胞肺癌（NSCLC）的信息很少。(2)研究方法：采用Western blot和免疫荧光法检测人NSCLC细胞系A549和人胚肺成纤维细胞MRC-5中组织蛋白酶K的表达。分别使用重组质粒和siRNA转染瞬时过表达或敲低组织蛋白酶K，以测试对细胞增殖、迁移、侵袭和对雷帕霉素（mTOR）信号传导通路的哺乳动物靶标的影响。(3)结果如下：与MRC-5细胞相比，A549细胞中组织蛋白酶K的表达显著增加，并且在细胞质中扩散。组织蛋白酶K过表达促进A549细胞增殖、迁移和侵袭，并伴有mTOR激活。下调Cathepsin K可逆转上述恶性行为，抑制mTOR信号通路的激活，提示Cathepsin K可能通过激活mTOR信号通路促进NSCLC的进展。(4)结论：组织蛋白酶K可能是治疗非小细胞肺癌的一个可行的药物靶点。
(1) Background: Cathepsin K has been found overexpressed in several malignant tumors. However, there is little information regarding the involvement of Cathepsin K in non-small cell lung cancer (NSCLC). (2) Methods: Cathepsin K expression was tested in human NSCLC cell lines A549 and human embryo lung fibroblast MRC-5 cells using Western blot and immunofluorescence assay. Cathepsin K was transiently overexpressed or knocked down using transfection with a recombinant plasmid and siRNA, respectively, to test the effects on cell proliferation, migration, invasion, and on the mammalian target of rapamycin (mTOR) signaling pathway. (3) Results: Expression of Cathepsin K was increased significantly in A549 cells and diffused within the cytoplasm compared to the MRC-5 cells used as control. Cathepsin K overexpression promoted the proliferation, migration, and invasion of A549 cells, accompanied by mTOR activation. Cathepsin K knockdown reversed the above malignant behavior and inhibited the mTOR signaling activation, suggesting that Cathepsin K may promote the progression of NSCLC by activating the mTOR signaling pathway. (4) Conclusion: Cathepsin K may potentially represent a viable drug target for NSCLC treatment.
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