MP39-17 MECP2 Silencing in high grade bladder Cancer derived HTB-5 Cell line affects Cellular Proliferation and Migratory ability

Shumaila Bilgrami; Zulfiqar Naqvi; Khalid Shaikh; El-Nasir Lalani; Farhat Abbas

MP39-17 MECP2 Silencing in high grade bladder Cancer derived HTB-5 Cell line affects Cellular Proliferation and Migratory ability

Shumaila Bilgrami, Zulfiqar Naqvi, Khalid Shaikh, El-Nasir Lalani, Farhat Abbas

Research output: Contribution to journal › Article

Abstract

DNA methylation patterns and chromatin structure is significantly altered in many human neoplasms including bladder cancer. Aberrant promoter hypermethylation of tumor suppressor genes is now a well established mechanism of gene inactivation. Methyl binding proteins are believed to act as interpreters of DNA methylation signal. The methyl binding protein MeCP2 has been shown to bind specifically to the 5mCpGs that are flanked by A/T residues. (Klose R et al., 2005) and mediates transcriptional repression by recruiting histone deacetylases (Adrian Bird at al.,1998) and thus, serving as a bridge between two major regulatory mechanisms of gene expression-DNA methylation and histone deacetylation.

Original language	Undefined/Unknown
Journal	Department of Pathology and Laboratory Medicine
Publication status	Published - 1 Apr 2014

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http://ecommons.aku.edu/pakistan_fhs_mc_pathol_microbiol/433

Cite this

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title = "MP39-17 MECP2 Silencing in high grade bladder Cancer derived HTB-5 Cell line affects Cellular Proliferation and Migratory ability",

abstract = "DNA methylation patterns and chromatin structure is significantly altered in many human neoplasms including bladder cancer. Aberrant promoter hypermethylation of tumor suppressor genes is now a well established mechanism of gene inactivation. Methyl binding proteins are believed to act as interpreters of DNA methylation signal. The methyl binding protein MeCP2 has been shown to bind specifically to the 5mCpGs that are flanked by A/T residues. (Klose R et al., 2005) and mediates transcriptional repression by recruiting histone deacetylases (Adrian Bird at al.,1998) and thus, serving as a bridge between two major regulatory mechanisms of gene expression-DNA methylation and histone deacetylation.",

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T1 - MP39-17 MECP2 Silencing in high grade bladder Cancer derived HTB-5 Cell line affects Cellular Proliferation and Migratory ability

AU - Bilgrami, Shumaila

AU - Naqvi, Zulfiqar

AU - Shaikh, Khalid

AU - Lalani, El-Nasir

AU - Abbas, Farhat

PY - 2014/4/1

Y1 - 2014/4/1

N2 - DNA methylation patterns and chromatin structure is significantly altered in many human neoplasms including bladder cancer. Aberrant promoter hypermethylation of tumor suppressor genes is now a well established mechanism of gene inactivation. Methyl binding proteins are believed to act as interpreters of DNA methylation signal. The methyl binding protein MeCP2 has been shown to bind specifically to the 5mCpGs that are flanked by A/T residues. (Klose R et al., 2005) and mediates transcriptional repression by recruiting histone deacetylases (Adrian Bird at al.,1998) and thus, serving as a bridge between two major regulatory mechanisms of gene expression-DNA methylation and histone deacetylation.

AB - DNA methylation patterns and chromatin structure is significantly altered in many human neoplasms including bladder cancer. Aberrant promoter hypermethylation of tumor suppressor genes is now a well established mechanism of gene inactivation. Methyl binding proteins are believed to act as interpreters of DNA methylation signal. The methyl binding protein MeCP2 has been shown to bind specifically to the 5mCpGs that are flanked by A/T residues. (Klose R et al., 2005) and mediates transcriptional repression by recruiting histone deacetylases (Adrian Bird at al.,1998) and thus, serving as a bridge between two major regulatory mechanisms of gene expression-DNA methylation and histone deacetylation.

M3 - Article

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JF - Department of Pathology and Laboratory Medicine

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