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Updated: Mar 15, 2026

A Functional Assay for Gap Junctional Examination; Electroporation of Adherent Cells on Indium-Tin Oxide
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A Functional Assay for Gap Junctional Examination; Electroporation of Adherent Cells on Indium-Tin Oxide

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Eupatilin inhibits EGF-induced JB6 cell transformation by targeting PI3K

Feng Li1, Ya Tao1, Yan Qiao1

  • 1Department of Pathophysiology, Basic Medical College, Zhengzhou University, Zhengzhou, Henan 450001, P.R. China.

International Journal of Oncology
|August 31, 2016
PubMed

Insights

Eupatilin, a natural compound, inhibits skin cell transformation by targeting Phosphatidylinositol 3-kinases (PI3Ks). This study reveals eupatilin

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Phosphatidylinositol 3-kinases (PI3Ks) are crucial in cell signaling pathways.
  • Aberrant PI3K pathway activation is linked to cancer development and progression.
  • PI3K is a significant target for cancer chemoprevention and chemotherapy.

Purpose of the Study:

  • To investigate the direct molecular targets of eupatilin, a natural flavone, in cancer chemoprevention.
  • To determine if eupatilin can inhibit skin cell transformation.
  • To elucidate the mechanism by which eupatilin exerts its antitumor effects.

Main Methods:

  • Cell proliferation and colony formation assays using JB6 cells.
  • Western blotting to assess PI3K downstream signaling.
  • Computational docking and pull-down assays to identify eupatilin's binding target.
  • Cell cycle analysis.

Main Results:

  • Eupatilin suppressed JB6 cell proliferation and epidermal growth factor-induced colony formation.
  • Eupatilin treatment reduced phosphorylation of PI3K downstream signaling molecules.
  • Eupatilin induced G1 phase cell cycle arrest and downregulated cyclin D1 expression.
  • Computational and experimental assays confirmed eupatilin binds to the p110α catalytic subunit of PI3K.

Conclusions:

  • Eupatilin demonstrates potential as a chemopreventive agent against skin cell transformation.
  • The mechanism involves targeting and inhibiting the PI3K pathway.
  • Eupatilin's direct binding to PI3K's p110α subunit underlies its observed effects.

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