Asset Details
Do you wish to reserve the book?
HDAC inhibitors induce transcriptional repression of high copy number genes in breast cancer through elongation blockade
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
HDAC inhibitors induce transcriptional repression of high copy number genes in breast cancer through elongation blockade
Do you wish to request the book?
HDAC inhibitors induce transcriptional repression of high copy number genes in breast cancer through elongation blockade
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
HDAC inhibitors induce transcriptional repression of high copy number genes in breast cancer through elongation blockade
2013
Overview
Treatment with histone deacetylase inhibitors (HDACI) results in potent cytotoxicity of a variety of cancer cell types, and these drugs are used clinically to treat hematological tumors. They are known to repress the transcription of
ERBB2
and many other oncogenes, but little is known about this mechanism. Using global run-on sequencing (GRO-seq) to measure nascent transcription, we find that HDACI cause transcriptional repression by blocking RNA polymerase II elongation. Our data show that HDACI preferentially repress the transcription of highly expressed genes as well as high copy number genes in HER2+ breast cancer genomes. In contrast, genes that are activated by HDACI are moderately expressed. We analyzed gene copy number in combination with microarray and GRO-seq analysis of expression level, in normal and breast cancer cells to show that high copy number genes are more likely to be repressed by HDACI than non-amplified genes. The inhibition of transcription of amplified oncogenes, which promote survival and proliferation of cancer cells, might explain the cancer-specific lethality of HDACI, and may represent a general therapeutic strategy for cancer.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Analysis
/ Antineoplastic Agents - pharmacology
/ Female
/ Gene Expression Regulation, Neoplastic - drug effects
/ Gene Silencing - drug effects
/ Genes
/ Genomes
/ Histone Deacetylase Inhibitors - pharmacology
/ Humans
/ Hydroxamic Acids - pharmacology
/ Medicine
/ Oligonucleotide Array Sequence Analysis
/ Oncology
/ Receptor, ErbB-2 - metabolism
/ RNA Polymerase II - antagonists & inhibitors
/ RNA Polymerase II - metabolism
/ Transcription Elongation, Genetic - drug effects
/ Transcription Initiation, Genetic
/ Tumors
