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Induction and Analysis of Epithelial to Mesenchymal Transition
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Induction and Analysis of Epithelial to Mesenchymal Transition

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PEP06 polypeptide 30 exerts antitumour effect in colorectal carcinoma via inhibiting epithelial-mesenchymal

Siming Yu1, Linna Li2, Wei Tian1

  • 1Department of Pharmacology (The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), Harbin Medical University, Harbin, Heilongjiang, China.

British Journal of Pharmacology
|May 4, 2018
PubMed
Abstract

Insights

PEP06, a modified endostatin polypeptide, inhibits colorectal cancer (CRC) cell migration and metastasis. It targets integrin αvβ3 to down-regulate miR-146b-5p, thereby suppressing epithelial-mesenchymal transition (EMT) and improving survival.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Colorectal cancer (CRC) remains a significant health challenge.
  • Investigating novel therapeutic strategies is crucial for improving patient outcomes.
  • Endostatin derivatives show promise in preclinical cancer models.

Purpose of the Study:

  • To evaluate the antitumour effects of PEP06, a modified endostatin polypeptide, on colorectal cancer (CRC).
  • To elucidate the underlying mechanisms of PEP06's antitumour activity in vitro and in vivo.
  • To explore PEP06's potential as a therapeutic agent for CRC.

Main Methods:

  • Cell proliferation, migration, and epithelial-mesenchymal transition (EMT) assays were conducted in CRC cell lines.
  • Western blotting, immunofluorescence, and immunohistochemistry were used to assess EMT markers.
  • MiRNA expression profiling, in situ hybridization, and quantitative real-time PCR identified regulated miRNAs.
  • Biacore SA biochips analyzed PEP06-integrin αvβ3 interactions.
  • Gain- and loss-of-function studies validated miR-146b-5p's role.
  • A mouse model assessed PEP06's effect on lung metastasis.

Main Results:

  • PEP06 reduced CRC cell migration and EMT without affecting cell viability.
  • PEP06 suppressed miR-146b-5p expression by binding to integrin αvβ3.
  • The miR-146b-5p-Smad4 pathway was identified as a regulator of EMT in CRC.
  • PEP06 inhibited pulmonary metastasis, enhanced mouse survival, and reduced residual tumor growth.

Conclusions:

  • PEP06 inhibits CRC growth and metastasis by binding to integrin αvβ3, down-regulating miR-146b-5p, and suppressing EMT.
  • The RGD motif in PEP06 is critical for its interaction with integrin αvβ3.
  • PEP06 demonstrates potential as a novel therapeutic agent for colorectal cancer.

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