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Epigenetic Regulation01:37

Epigenetic Regulation

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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  6. Cthrc1 Modulates Cell Proliferation And Invasion In Hepatocellular Carcinoma By Dna Methylation.

CTHRC1 modulates cell proliferation and invasion in hepatocellular carcinoma by DNA methylation.

Xiangjun Sun1,2, Ye Liu2, Changdong Cheng2

  • 1Department of Hepatobiliary Surgery, Linyi People's Hospital, Linyi, 276000, China.

Discover Oncology
|August 12, 2024

Related Experiment Videos

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
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An Alternative Culture Method to Maintain Genomic Hypomethylation of Mouse Embryonic Stem Cells Using MEK Inhibitor PD0325901 and Vitamin C
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An Alternative Culture Method to Maintain Genomic Hypomethylation of Mouse Embryonic Stem Cells Using MEK Inhibitor PD0325901 and Vitamin C

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Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
09:42

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images

Published on: September 7, 2017

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View abstract on PubMed

Summary
This summary is machine-generated.

High expression of Collagen triple helix repeat containing-1 (CTHRC1) in liver cancer is linked to hypomethylation and promotes tumor growth. CTHRC1 influences angiogenesis, alternative splicing, and gene fusions in hepatocellular carcinoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Collagen triple helix repeat containing-1 (CTHRC1) is an extracellular matrix protein.
  • CTHRC1 is highly expressed in hepatocellular carcinoma (HCC), correlating with poor patient prognosis.
  • The specific mechanisms by which CTHRC1 contributes to HCC progression remain largely undefined.

Purpose of the Study:

  • To elucidate the role and underlying mechanisms of CTHRC1 in hepatocellular carcinoma (HCC) development.
  • To investigate the relationship between CTHRC1 expression, methylation status, and cellular functions in HCC.
  • To identify molecular pathways, including angiogenesis, alternative splicing, and gene fusions, associated with CTHRC1 activity in HCC.

Main Methods:

  • Agena MassARRAY® Methylation Analysis was used to quantify CTHRC1 promoter methylation.
Keywords:
AngiogenesisCollagen triple helix repeat containing-1DNA methylationHepatocellular carcinoma

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Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
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  • Functional assays, including cell proliferation, migration, and invasion assays, were performed after CTHRC1 knockdown in Hep3B2.1 cells.
  • RNA sequencing, rMATS, and Arriba were employed to analyze gene expression, lncRNAs, alternative splicing, and gene fusions.
  • Main Results:

    • CTHRC1 exhibited high expression and hypomethylation in HCC cell lines.
    • CTHRC1 downregulation significantly inhibited HCC cell proliferation, migration, invasion, and induced G1/S phase arrest and apoptosis.
    • RNA sequencing identified differentially expressed angiogenesis-related mRNAs and lncRNAs, aberrant expression of specific genes (e.g., CXCL6, LINC02127), 12 alternative splicing events, and 5 gene fusion pairs associated with CTHRC1 activity.

    Conclusions:

    • Elevated CTHRC1 expression, associated with hypomethylation, promotes HCC progression.
    • CTHRC1's oncogenic role in HCC involves modulation of angiogenesis, alternative splicing, and gene fusion events.
    • Targeting CTHRC1 may offer a therapeutic strategy for hepatocellular carcinoma.