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首页> 外文期刊>Journal of cellular physiology. >TRB3 interacts with ERK and JNK and contributes to the proliferation, apoptosis, and migration of lung adenocarcinoma cells
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TRB3 interacts with ERK and JNK and contributes to the proliferation, apoptosis, and migration of lung adenocarcinoma cells

机译：TRB3 ERK和物相互作用的贡献增殖、凋亡、迁移肺腺癌的细胞

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摘要

Tribbles homolog 3 (TRB3) has been accounted for regulation of a few cell processes through interaction with other significant proteins. The molecular mechanisms underlying TRB3 in tumorigenesis in lung adenocarcinoma have not been entirely elucidated. The present study is aimed at determining the function and fundamental mechanisms of TRB3 in lung adenocarcinoma progression. TRB3 was highly expressed in A549 and H1299 cells and lung adenocarcinoma tissues compared with human bronchial epithelial cells (HBEpC) and adjacent normal lung tissues. Hypoxia significantly upregulated the expression of TRB3 protein in A549 and H1299 cells in a time-dependent way. Gene expression profiling interactive analysis data analysis indicated that patients with lung adenocarcinoma with excessive expression of TRB3 mRNA had fundamentally shorter survival time. TRB3 knockdown in A549 cells can inhibit cell proliferation and migration, and promote cell apoptosis. TRB3 knockdown reduced the expression of p-ERK and p-JNK, but did not affect the expression of p-P38 MAPK. TRB3 overexpression enhances the malignant transformation abilities of HBEpC such as cell proliferation, migration and colony formation, which could be reversed by U0126 and SP600125. TRB3 overexpression promotes the phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) but was not affected by U0126 and SP600125. The results of coimmunoprecipitation experiments indicated that TRB3 binds directly to ERK and JNK. This study suggests that TRB3 has a potentially carcinogenic role in lung adenocarcinoma by binding to ERK and JNK and promoting the phosphorylation of ERK and JNK. TRB3 can be a possible therapeutic focus for lung adenocarcinoma.
机译：毛球族同族体3 (TRB3)已经占了通过调节一些细胞过程互动与其他重要的蛋白质。TRB3分子机制肿瘤发生在肺腺癌完全阐明。旨在确定和基本功能在肺腺癌TRB3机制进展。和H1299细胞和肺腺癌组织相比之下,人类支气管上皮细胞(HBEpC)和相邻的正常肺组织。显著调节TRB3的表达蛋白质在A549和H1299细胞时间的方式。数据分析表明,交互式分析肺腺癌患者过度TRB3 mRNA的表达从根本上更短生存时间。抑制细胞增殖和迁移促进细胞凋亡。的表达p-ERK p-JNK,但是没有影响的表达p-P38 MAPK。超表达增强了恶性转换HBEpC如细胞的能力增殖、迁移和集落形成,这可能被U0126和SP600125逆转。TRB3超表达促进磷酸化细胞外signal-regulated激酶(ERK)c-Jun n端激酶(物),但并没有受U0126 SP600125。coimmunoprecipitation实验表明,TRB3直接绑定到ERK和物。表明TRB3有可能致癌在肺腺癌绑定ERK和作用物和促进ERK的磷酸化和物。肺腺癌。

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