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Publication
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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 |
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Month |
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Year of Publication |
2022 |
Page |
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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 |
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Reviewing Status |
มีผู้ประเมินอิสระ |
Status |
ได้รับการตอบรับให้ตีพิมพ์ |
Level of Publication |
นานาชาติ |
citation |
false |
Part of thesis |
true |
Attach file |
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Citation |
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