摘要
背景:以前,我们发现含锌指的转录因子znf 424抑制了p21的转录,而p21的转录与多种肿瘤的发生有广泛的联系,但由于znf 424在肺癌发生中的作用尚不明确,因此我们将znf 424的表达与肺癌的发生发展联系起来。 结果:60例肺癌组织中有43例znf 424表达明显低于癌旁组织,流式细胞仪检测显示znf 424过表达可诱导A 549人肺癌细胞凋亡,过表达znf 424可显著增加G1期细胞数,减少S期细胞数,提示znf 424抑制肺癌细胞增殖。Westernblot分析表明,过表达znf 424可降低A 549细胞丝裂原活化蛋白激酶(MAPK)信号蛋白p-p38和p-erk的蛋白表达水平。 结论:znf 424与肺癌的发生有关,在肺癌中有一定的抑制作用,提示znf 424的表达有可能作为肺癌发生的诊断指标。
关键词: ZNF424,肺癌,凋亡,MAPK通路。
Current Molecular Medicine
Title:ZNF424 Induces Apoptosis and Inhibits Proliferation in Lung Carcinoma Cells
Volume: 18 Issue: 2
关键词: ZNF424,肺癌,凋亡,MAPK通路。
摘要: Background: Previously, we showed that the Zinc finger-containing transcription factor ZNF424 inhibits p21 transcription, which has been widely associated with various cancers. However, because the roles of ZNF424 in tumorigenesis have not been characterized, we correlated ZNF424 expression with tumorigenesis in lung cancer.
Results: The present immunohistochemical analyses show significantly lower ZNF424 expression levels in 43 of 60 lung cancer tissues compared with adjacent tissues. Moreover, flow cytometry assays indicated that overexpression of ZNF424 induces apoptosis in A549 human lung carcinoma cells, and overexpression of ZNF424 significantly increases numbers of G1 phase cells and decreases numbers of S phase cells, suggesting that ZNF424 inhibits proliferation. Western Blot analyses show that overexpression of ZNF424 decreases protein expression levels of the mitogen-activated protein kinase (MAPK) signaling proteins P-P38 and P-ERK in A549 cells.
Conclusion: These are the first data to associate ZNF424 with tumorigenesis and demonstrate an inhibitory role in lung cancer, indicating the potential of ZNF424 expression as a diagnostic marker of lung tumorigenesis.
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Cite this article as:
ZNF424 Induces Apoptosis and Inhibits Proliferation in Lung Carcinoma Cells, Current Molecular Medicine 2018; 18 (2) . https://dx.doi.org/10.2174/1566524018666180705113642
DOI https://dx.doi.org/10.2174/1566524018666180705113642 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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