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Updated: Oct 20, 2025

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate
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A c-Met Inhibitor Suppresses Osteosarcoma Progression via the ERK1/2 Pathway in Human Osteosarcoma Cells

Weijie Chen1,2,3, Su Wu4, Yang Huang3

  • 1Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, HangZhou, People's Republic of China.

Oncotargets and Therapy
|September 17, 2021
PubMed
Abstract

Insights

The c-Met inhibitor PHA-665752 shows promise in treating osteosarcoma by suppressing tumor growth and promoting apoptosis. This study highlights Met as a druggable target for developing new osteosarcoma therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Osteosarcoma, a common bone cancer in children and adolescents, has a poor prognosis due to metastasis and drug resistance.
  • The HGF/c-Met signaling pathway is implicated in various cancers, presenting a potential therapeutic target.

Purpose of the Study:

  • To investigate the role of Met as a cancer-promoting gene in osteosarcoma.
  • To evaluate the efficacy of the c-Met inhibitor PHA-665752 in osteosarcoma treatment.

Main Methods:

  • In vitro studies using human osteosarcoma cell lines (143B, U2OS) treated with PHA-665752.
  • Assays included CCK8 for IC50, colony formation, transwell migration/invasion, and wound healing.
  • In vivo experiments utilized a tumor-transplanted mouse model.

Main Results:

  • PHA-665752 inhibited osteosarcoma cell proliferation, migration, and invasion, while promoting apoptosis.
  • The ERK1/2 pathway was identified as a key mediator of PHA-665752's anti-cancer effects.
  • PHA-665752 demonstrated significant tumor growth suppression in vivo.

Conclusions:

  • Met is a druggable target in osteosarcoma.
  • PHA-665752 is a potential therapeutic agent for osteosarcoma treatment.
Keywords:
ERK signalingLY3214996MetPHA-665752osteosarcoma

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