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Transcription Elongation Factors02:35

Transcription Elongation Factors

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Transcription elongation is a dynamic process that alters depending upon the sequence heterogeneity of the DNA being transcribed. Hence, it is not surprising that the elongation complex's composition also varies along the way while transcribing a gene.
The transcription elongation is regulated via pausing of RNA polymerase on several occasions during transcription. In bacteria, these halts are necessary because the transcription of DNA into mRNA is coupled to the translation of that mRNA...
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
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Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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Transcription01:10

Transcription

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Overview
Transcription is the process of synthesizing RNA from a DNA sequence by RNA polymerase. It is the first step in producing a protein from a gene sequence. Additionally, many other proteins and regulatory sequences are involved in the proper synthesis of messenger RNA (mRNA). Regulation of transcription is responsible for the differentiation of all the different types of cells and often for the proper cellular response to environmental signals.
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Artificial RNA Polymerase II Elongation Complexes for Dissecting Co-transcriptional RNA Processing Events
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Targeting Processive Transcription Elongation via SEC Disruption for MYC-Induced Cancer Therapy.

Kaiwei Liang1, Edwin R Smith2, Yuki Aoi1

  • 1Simpson Querrey Center for Epigenetics, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Biochemistry and Molecular Genetics, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.

Cell
|October 20, 2018
PubMed
Summary
This summary is machine-generated.

Researchers discovered compounds KL-1 and KL-2 that inhibit the super elongation complex (SEC). This inhibition impacts transcription, heat-shock response, and MYC activity, showing potential for treating MYC-driven cancers.

Keywords:
MYCSECprocessive elongationpromoter-proximal pausingsuper elongation complextranscription elongationtranscriptional addiction in cancer

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Area of Science:

  • Molecular Biology
  • Biochemistry
  • Cancer Research

Background:

  • The super elongation complex (SEC) is crucial for efficient gene transcription by facilitating RNA polymerase II (Pol II) release and processivity.
  • SEC dysfunction is implicated in various human diseases, including cancer.

Purpose of the Study:

  • To identify small molecules that disrupt SEC function.
  • To investigate the therapeutic potential of SEC inhibitors in cancer.

Main Methods:

  • Identification of peptidomimetic lead compounds KL-1 and KL-2.
  • Assessing the impact of KL-1 and KL-2 on Pol II release and transcription elongation rates.
  • Evaluating the effect of SEC inhibition on heat-shock gene induction across species.
  • Analyzing the downregulation of MYC and MYC-dependent genes.
  • Testing efficacy in a mouse xenograft model of MYC-driven cancer.

Main Results:

  • KL-1 and KL-2 were identified as compounds that disrupt the AFF4-P-TEFb interaction within SEC.
  • These compounds impair Pol II release from pause sites and reduce transcription elongation rates.
  • SEC inhibition by KL-1 and KL-2 attenuates the heat-shock response in both Drosophila and human cells.
  • Inhibition of SEC downregulates MYC and its downstream transcriptional targets in mammalian cells.
  • Treatment with KL-1 and KL-2 delayed tumor progression in a mouse model of MYC-driven cancer.

Conclusions:

  • Small-molecule inhibitors targeting SEC, such as KL-1 and KL-2, can effectively impair transcription and cellular stress responses.
  • SEC inhibition demonstrates therapeutic potential for treating MYC-driven cancers by downregulating oncogenic transcription programs.