Abstract:
:The poor outcome of hepatocellular carcinoma (HCC) is mainly due to the development of fast growth, invasion and metastasis. The role of TET2 has been implicated in some cancer types, but its role and mechanisms in HCC remains elusive. In this study, our findings indicated that TET2 expression frequently increased in HCC and that TET2 expressional upregulation correlated with HCC progression. TET2 knockdown inhibited HCC cells proliferation in vitro and growth in vivo, and inhibited the invasion potential of HCC cells. Mechanically, TET2 knockdown upregulated E-cadherin expression and then attenuated β-catenin transactivation in HCC cells. TET2 repressed E-cadherin expression via recruited HDAC1 to E-cadherin promoter to reduce the H3K9Ac and H4K16Ac levels. Moreover, β-catenin signaling transcriptionally regulated TET2 expression to form a positive feedback in HCC cells. These findings indicate that the dysregulation of TET2/E-cadherin/β-catenin regulatory loop is a critical oncogenic event in HCC progression.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Yang G,Zeng X,Wang M,Wu Adoi
10.1016/j.yexcr.2018.01.011subject
Has Abstractpub_date
2018-02-15 00:00:00pages
218-226issue
2eissn
0014-4827issn
1090-2422pii
S0014-4827(18)30012-0journal_volume
363pub_type
杂志文章abstract::Hypoxia inducible factor 1 (HIF-1), the key mediator of hypoxia signaling pathways, has been shown involved in hypoxia-induced radioresistance. However, the underlying mechanisms are unclear. The present study demonstrated that both hypoxia and hypoxia mimetic cobalt chloride could increase the radioresistance of huma...
journal_title:Experimental cell research
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journal_title:Experimental cell research
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journal_title:Experimental cell research
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