We are analyzing https://link.springer.com/article/10.1007/s12032-016-0734-z.

Title:
Epigenetic regulation of E-cadherin expression by the histone demethylase UTX in colon cancer cells | Medical Oncology
Description:
Decreased epithelial cadherin (E-cadherin) gene expression, a hallmark of epithelial–mesenchymal transition (EMT), is essential for triggering metastatic advantage of the colon cancer. Genetic mechanisms underlying the regulation of E-cadherin expression in EMT have been extensively investigated; however, much is unknown about the epigenetic mechanism underlying this process. Here, we identified ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX), a histone demethylase involved in demethylating di- or tri-methylated histone 3 lysine 27 (H3K27me2/3), as a positive regulator for the expression of E-cadherin in the colon cancer cell line HCT-116. We showed that inactivation of UTX down-regulated E-cadherin gene expression, while overexpression of UTX did the opposite. Notably, overexpression of UTX inhibited migration and invasion of HCT-116 cells. Moreover, UTX demethylated H3K27me3, a histone transcriptional repressive mark, leading to decreased H3K27me3 at the E-cadherin promoter. Further, UTX interacted with the histone acetyltransferase (HAT) protein CBP and recruited it to the E-cadherin promoter, resulting in increased H3K27 acetylation (H3K27ac), a histone transcriptional active mark. UTX positively regulates E-cadherin expression through coordinated regulation of H3K27 demethylation and acetylation, switching the transcriptional repressive state to the transcriptional active state at the E-cadherin promoter. We conclude that UTX may play a role in regulation of E-cadherin gene expression in HCT-116 cells and that UTX may serve as a therapeutic target against the metastasis in the treatment of colon cancer.
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Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, cell, histone, central, ecadherin, regulation, utx, cells, epithelialmesenchymal, transition, expression, methylation, wang, epigenetic, colon, biol, mol, demethylase, zha, shi, lysine, acetylation, metastasis, access, dna, human, nature, usa, privacy, cookies, content, gene, transcriptional, protein, med, oncol, publish, search, cui, xue, hct, repressive, state, role, clin,

Topics {✒️}

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         headline:Epigenetic regulation of E-cadherin expression by the histone demethylase UTX in colon cancer cells
         description:Decreased epithelial cadherin (E-cadherin) gene expression, a hallmark of epithelial–mesenchymal transition (EMT), is essential for triggering metastatic advantage of the colon cancer. Genetic mechanisms underlying the regulation of E-cadherin expression in EMT have been extensively investigated; however, much is unknown about the epigenetic mechanism underlying this process. Here, we identified ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX), a histone demethylase involved in demethylating di- or tri-methylated histone 3 lysine 27 (H3K27me2/3), as a positive regulator for the expression of E-cadherin in the colon cancer cell line HCT-116. We showed that inactivation of UTX down-regulated E-cadherin gene expression, while overexpression of UTX did the opposite. Notably, overexpression of UTX inhibited migration and invasion of HCT-116 cells. Moreover, UTX demethylated H3K27me3, a histone transcriptional repressive mark, leading to decreased H3K27me3 at the E-cadherin promoter. Further, UTX interacted with the histone acetyltransferase (HAT) protein CBP and recruited it to the E-cadherin promoter, resulting in increased H3K27 acetylation (H3K27ac), a histone transcriptional active mark. UTX positively regulates E-cadherin expression through coordinated regulation of H3K27 demethylation and acetylation, switching the transcriptional repressive state to the transcriptional active state at the E-cadherin promoter. We conclude that UTX may play a role in regulation of E-cadherin gene expression in HCT-116 cells and that UTX may serve as a therapeutic target against the metastasis in the treatment of colon cancer.
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         dateModified:2016-01-27T00:00:00Z
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            H3K27
            UTX
            EMT
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            Colon cancer
            Oncology
            Hematology
            Pathology
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      headline:Epigenetic regulation of E-cadherin expression by the histone demethylase UTX in colon cancer cells
      description:Decreased epithelial cadherin (E-cadherin) gene expression, a hallmark of epithelial–mesenchymal transition (EMT), is essential for triggering metastatic advantage of the colon cancer. Genetic mechanisms underlying the regulation of E-cadherin expression in EMT have been extensively investigated; however, much is unknown about the epigenetic mechanism underlying this process. Here, we identified ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX), a histone demethylase involved in demethylating di- or tri-methylated histone 3 lysine 27 (H3K27me2/3), as a positive regulator for the expression of E-cadherin in the colon cancer cell line HCT-116. We showed that inactivation of UTX down-regulated E-cadherin gene expression, while overexpression of UTX did the opposite. Notably, overexpression of UTX inhibited migration and invasion of HCT-116 cells. Moreover, UTX demethylated H3K27me3, a histone transcriptional repressive mark, leading to decreased H3K27me3 at the E-cadherin promoter. Further, UTX interacted with the histone acetyltransferase (HAT) protein CBP and recruited it to the E-cadherin promoter, resulting in increased H3K27 acetylation (H3K27ac), a histone transcriptional active mark. UTX positively regulates E-cadherin expression through coordinated regulation of H3K27 demethylation and acetylation, switching the transcriptional repressive state to the transcriptional active state at the E-cadherin promoter. We conclude that UTX may play a role in regulation of E-cadherin gene expression in HCT-116 cells and that UTX may serve as a therapeutic target against the metastasis in the treatment of colon cancer.
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         Colon cancer
         Oncology
         Hematology
         Pathology
         Internal Medicine
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            name:Georgia State University
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      affiliation:
            name:Georgia State University
            address:
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               type:PostalAddress
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      name:Fenfen Li
      affiliation:
            name:Georgia State University
            address:
               name:Department of Biology and Center for Obesity Reversal, Georgia State University, Atlanta, USA
               type:PostalAddress
            type:Organization
      name:Houjie Liang
      affiliation:
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      name:Department of Biology and Center for Obesity Reversal, Georgia State University, Atlanta, USA
      name:Department of Oncology and Southwest Cancer Center, Southwest Hospital, The Third Military Medical University, Chongqing, China
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