2012 ©
             Publication
Journal Publication
Title of Article HMGN3 represses transcription of epithelial regulators to promote migration of cholangiocarcinoma in a SNAI2-dependent manner 
Date of Acceptance 28 April 2022 
Journal
     Title of Journal Federation of American Societies for Experimental Biology 
     Standard SCOPUS 
     Institute of Journal Wiley Online Library 
     ISBN/ISSN 1530-6860 
     Volume 2022 
     Issue  
     Month
     Year of Publication 2022 
     Page  
     Abstract High mobility group nucleosome binding protein 3 (HMGN3), a member of the HMGN family, modulates the structure of chromatin and regulates transcription through transcription factors. HMGN3 has been implicated in the development of various cancers; however, the underlying mechanisms remain unclear. We herein demonstrated that the high expression of HMGN3 correlated with the metastasis of liver fluke infection-induced cholangiocarcinoma (CCA) in patients in northeastern Thailand. The knockdown of HMGN3 in CCA cells significantly impaired the oncogenic properties of colony formation, migration, and invasion. HMGN3 inhibited the expression of and blocked the intracellular polarities of epithelial regulator genes, such as the CDH1/E-cadherin and TJAP1 genes in CCA cell. A chromatin immunoprecipitation sequencing analysis revealed that HMGN3 required the transcription factor SNAI2 to bind to and repress the expression of epithelial regulator genes, at least in part, due to histone deacetylases (HDACs), the pharmacological inhibition of which reactivated these epithelial regulators in CCA, leading to impairing the cell migration capacity. Therefore, the overexpression of HMGN3 represses the transcription of and block the polarities of epithelial regulators in CCA cells in a manner that is dependent on the SNAI2 gene and HDACs. 
     Keyword HMGN, Transcription factor, Epithelial mesenchymal transition, Histone deacetylase, Liver fluke 
Author
605070004-0 Miss SUPANNIKA SORIN [Main Author]
Medicine Master's Degree

Reviewing Status มีผู้ประเมินอิสระ 
Status ได้รับการตอบรับให้ตีพิมพ์ 
Level of Publication นานาชาติ 
citation false 
Part of thesis true 
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