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Imazamethabenz inhibits human breast cancer cell proliferation, migration and invasion via combination with Pin1

Chen Liu1, Chaoyu Mu1, Zeng Li1

  • 1College of Pharmacy, Anhui Medical University, Hefei, Anhui 230032, P.R. China.

Molecular Medicine Reports
|March 29, 2017
PubMed

Insights

The herbicide imazamethabenz inhibits peptidyl-prolyl cis/trans isomerase, NIMA interacting‑1 (Pin1), a key marker in tumor development. This compound shows potential as an antitumor drug by inducing apoptosis and inhibiting breast cancer cell migration and invasion.

Area of Science:

  • Biochemistry
  • Oncology
  • Drug Discovery

Background:

  • Overexpression of peptidyl-prolyl cis/trans isomerase, NIMA interacting‑1 (Pin1) is linked to tumor occurrence and progression.
  • Pin1 plays a crucial role in cancer cell signaling pathways.

Purpose of the Study:

  • To investigate the potential of the herbicide imazamethabenz as an antitumor agent by targeting Pin1.
  • To elucidate the mechanism by which imazamethabenz affects cancer cells.

Main Methods:

  • Molecular docking and in vitro enzyme activity assays to confirm Pin1 inhibition.
  • MTT assays, western blotting, wound healing, and Matrigel invasion assays on MCF-7 breast cancer cells.

Main Results:

  • Imazamethabenz was confirmed to effectively inhibit Pin1 in vitro.
  • The compound induced apoptosis and suppressed migration and invasion in MCF-7 cells.
  • Inhibition of Pin1-mediated signaling pathways involving VEGF and MMP-9 was observed.

Conclusions:

  • Imazamethabenz demonstrates significant antitumor potential by inhibiting Pin1.
  • This herbicide offers a novel therapeutic strategy for treating Pin1-overexpressing tumors.

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