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Review
. 2013 Apr;16(4):211-5.
doi: 10.3779/j.issn.1009-3419.2013.04.07.

[Research advance on mechanism and application of HATs and HDACs in epithelial-mesenchymal transition of lung cancer]

[Article in Chinese]
Rui Chang  1 , Jiacong You, Qinghua Zhou
Affiliations
Review

[Research advance on mechanism and application of HATs and HDACs in epithelial-mesenchymal transition of lung cancer]

[Article in Chinese]
Rui Chang et al. Zhongguo Fei Ai Za Zhi. 2013 Apr.

Abstract
in English, Chinese

Lung cancer is one of the most common diseases that endanger health and life of people domestically. A number of recurrence and death of lung cancer originated from metastasis. As a key step in metastasis of lung cancer, epithelial to mesenchymal transition involved down-regulation of E-cadherin, as well as regulated by EMT transcription factors. HATs and HDACs is a protein family that catalyzes acetylation and deacetylation of histones. Not only they have vital functions in tumor pathogenesis, but also participate in the EMT of lung cancer. HATs and HDACs interact with certain EMT transcription factors. Moreover, the function of these EMT transcription factors may be regulated by acetylation, which has influence on EMT program in lung cancer. Therefore, this review introduces the event of HATs and HDACs function in EMT of lung cancer, and investigate the molecular mechanism of their interaction. Then, the potential of HDAC inhibitor utilization in the inhibition of EMT and lung cancer therapy were discussed, as to pave the way for the related basic research and clinical practice.

肺癌是危害我国人民健康与生命的重大疾病之一，肺癌的复发和死亡多源于肿瘤转移。上皮细胞的间质化过程（epithelial-mesenchymal transition, EMT）是肺癌转移中的一个关键步骤，此过程涉及E-cadherin表达下调，并受到EMT转录因子调控。组蛋白乙酰转移酶（histone acetyltransferases, HATs）和组蛋白去乙酰化酶（histone deacetyltransferases, HDACs）是催化组蛋白乙酰化和去乙酰化的蛋白家族，不仅在肿瘤进程中发挥重要功能，近年来发现它们同样参与肺癌EMT过程。HATs与HDACs和某些EMT转录因子有相互作用。而且，这些EMT转录因子的功能受乙酰化调控，并影响肺癌EMT进程。本文将分别介绍HATs和HDACs参与肺癌EMT的作用机理，从分子机制方面对它们之间的相互作用进行探讨，并讨论HDAC抑制剂在抑制EMT和肺癌治疗方面的潜在应用价值，以期为相关基础研究和临床实践提供借鉴。

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References

    1. Pena C, Garcia JM, Garcia V, et al. The expression levels of the transcriptional regulators p300 and CtBP modulate the correlations between SNAIL, ZEB1, E-cadherin and vitamin D receptor in human colon carcinomas. Int J Cancer. 2006;119(9):2098–2104. doi: 10.1002/ijc.22083. - DOI - PubMed
    1. Yokomizo C, Yamaguchi K, Itoh Y, et al. High expression of p300 in HCC predicts shortened overall survival in association with enhanced epithelial mesenchymal transition of HCC cells. Cancer Lett. 2011;310(2):140–147. doi: 10.1016/j.canlet.2011.06.030. - DOI - PubMed
    1. Hsu YL, Huang MS, Yang CJ, et al. Lung tumor-associated osteoblast-derived bone morphogenetic protein-2 increased epithelial-to-mesenchymal transition of cancer by Runx2/Snail signaling pathway. J Biol Chem. 2011;286(43):37335–37346. doi: 10.1074/jbc.M111.256156. - DOI - PMC - PubMed
    1. Mu Y, Sundar R, Thakur N, et al. TRAF6 ubiquitinates TGFbeta type Ⅰ receptor to promote its cleavage and nuclear translocation in cancer. Nat Commun. 2011;2:330. doi: 10.1038/ncomms1332. - DOI - PMC - PubMed
    1. Hamamori Y, Sartorelli V, Ogryzko V, et al. Regulation of histone acetyltransferases p300 and PCAF by the bHLH protein twist and adenoviral oncoprotein E1A. Cell. 1999;96(3):405–413. doi: 10.1016/S0092-8674(00)80553-X. - DOI - PubMed

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