Trim28 Contributes to EMT via Regulation of E-Cadherin and N-Cadherin in Lung Cancer Cell Lines

被引:72
作者
Chen, Lu [1 ]
Munoz-Antonia, Teresita [1 ]
Cress, W. Douglas [1 ]
机构
[1] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Mol Oncol Program, Tampa, FL 33612 USA
来源
PLOS ONE | 2014年 / 9卷 / 07期
关键词
EPITHELIAL-MESENCHYMAL TRANSITION; ZINC-FINGER PROTEINS; GROWTH-FACTOR-BETA; GENE-EXPRESSION; TRANSCRIPTION; METASTASIS; COMPLEXES; KAP-1; PHOSPHORYLATION; ADENOCARCINOMA;
D O I
10.1371/journal.pone.0101040
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
In previous work, we demonstrated that transcription factor Trim28 (Tripartite motif containing 28) plays a tumor-suppressor role in early-staged adenocarcinoma of the lung due to its ability to restrain transcription of cell cycle-regulating genes. Herein we examine Trim28's role in the epithelial-to-mesenchymal transition (EMT) which is strongly implicated in cancer metastasis. We found that Trim28 plays a role in TGF-beta-induced EMT in non-small cell lung cancer cells. Silencing Trim28 with inhibitory RNAs alters the expression of numerous EMT markers, such as E-cadherin and N-cadherin, whereas overexpression of Trim28 has an opposite effect. Trim28 expression is induced following TGF-beta treatment at both protein and mRNA levels. Trim28 deficiency impairs TGF-beta-induced EMT and decreases cell migration and invasion. Finally, we demonstrate that the expression of Trim28 affects the acetylation and methylation of histones on E-cadherin and N-cadherin promoters. These results suggest that Trim28 contributes to EMT and might be important for tumor metastasis in lung cancer. Taken together with our previous work these results suggest a model in which Trim28 is a tumor suppressor early in the transformation process in lung cancer, but in later stages it functions as an oncogene.
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页数:10
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