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Proofreading01:31

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Synthesis of new DNA molecules is carried out by the enzyme DNA polymerase, which adds nucleotides on the daughter strand complementary to the template DNA strand. DNA polymerase has a higher affinity to add the correct base and ensures fidelity during DNA replication. Furthermore,  it exhibits proofreading activity during replication, using an exonuclease domain that cuts off incorrect nucleotides from the nascent DNA strand.
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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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The trp operon in Escherichia coli exemplifies a repressible operon. It regulates the synthesis of tryptophan through repressor-mediated transcriptional control and attenuation. This dual regulatory mechanism ensures tryptophan biosynthesis occurs only when needed, conserving cellular resources.Structure of the trp OperonThe trp operon consists of five structural genes (trpE, trpD, trpC, trpB, and trpA) that encode enzymes for tryptophan biosynthesis. These genes are transcribed as a single...
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Related Experiment Video

Updated: Nov 12, 2025

Transcorporal Artificial Urinary Sphincter Cuff Placement in a Case Requiring Revision for Urethral Atrophy
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Erratum.

Juan Gu1, Chang-Fu Cui2, Li Yang3

  • 1Department of Clinical Pharmacy, West China School of Pharmacy, Sichuan University, Sichuan, P.R. China.

Oncology Research
|March 18, 2021
PubMed
Summary
This summary is machine-generated.

Emodin, a natural compound, effectively inhibits colon cancer (CC) cell invasion and migration. It works by blocking epithelial-mesenchymal transition (EMT) through the Wnt/β-catenin pathway, offering potential for CC treatment.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Colon cancer (CC) is a major global health concern.
  • Emodin, an anthraquinone, shows potential in affecting tumor progression.
  • Understanding emodin's mechanism against CC invasion and migration is crucial.

Purpose of the Study:

  • To investigate the effects of emodin on colon cancer cell invasion and migration.
  • To elucidate the underlying molecular mechanisms, including epithelial-mesenchymal transition (EMT) and Wnt/β-catenin signaling.
  • To evaluate emodin's antitumor efficiency in vivo.

Main Methods:

  • In vitro studies using RKO colon cancer cells to assess invasion, migration, and gene expression.
  • In vivo studies using a colon cancer xenograft model.
  • Analysis of key proteins and genes involved in EMT and Wnt/β-catenin pathway.

Main Results:

  • Emodin significantly inhibited colon cancer cell invasion and migration in a dose-dependent manner.
  • Emodin decreased matrix metalloproteinase-7 (MMP-7), MMP-9, and vascular endothelial growth factor (VEGF) expression.
  • Emodin suppressed EMT by modulating E-cadherin, N-cadherin, Snail, and β-catenin, and inhibited the Wnt/β-catenin pathway.

Conclusions:

  • Emodin inhibits colon cancer cell invasion and migration by blocking EMT.
  • The Wnt/β-catenin signaling pathway is a key mediator of emodin's effects.
  • Emodin demonstrates antitumor potential in vivo by inhibiting EMT via the Wnt/β-catenin pathway.