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Updated: Feb 1, 2026

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Inhibiting GIT1 reduces the growth, invasion, and angiogenesis of osteosarcoma

Zitao Zhang1, Polu Hu2, Jin Xiong1

  • 1Department of Orthopedics, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, China, wsf0135@yeah.net.

Cancer Management and Research
|December 18, 2018
PubMed
Abstract

Insights

The scaffold protein GIT1 promotes osteosarcoma growth, invasion, and angiogenesis. Knocking down GIT1 inhibits these processes, suggesting GIT1 is an oncogenic factor and a potential therapeutic target for osteosarcoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • G protein-coupled receptor interacting protein 1 (GIT1) is a multi-domain scaffold protein implicated in various cellular functions.
  • While GIT1's role in several cancers is recognized, its specific function in osteosarcoma remains largely uncharacterized.
  • This study investigates the biological role and underlying mechanisms of GIT1 in osteosarcoma development.

Purpose of the Study:

  • To elucidate the function of GIT1 in osteosarcoma.
  • To determine the mechanism by which GIT1 influences osteosarcoma progression.
  • To evaluate GIT1 as a potential therapeutic target for osteosarcoma.

Main Methods:

  • Analysis of GIT1 expression in human osteosarcoma tissues.
  • In vitro studies using lentiviral knockdown of GIT1 in osteosarcoma cells to assess invasion and vascular endothelial growth factor (VEGF) release.
  • In vivo studies using an orthotopic femoral osteosarcoma model to evaluate tumor growth, invasion, and angiogenesis.
  • Western blot analysis to detect extracellular signal-regulated kinase (ERK1/2) activation and hypoxia-inducible factor-1 (HIF-1α) expression.

Main Results:

  • GIT1 is highly expressed in osteosarcoma tissues and cells.
  • Knockdown of GIT1 significantly inhibited osteosarcoma cell invasion and VEGF release in vitro.
  • GIT1 knockdown suppressed tumor growth, invasion, and angiogenesis in vivo.
  • GIT1 knockdown downregulated p-ERK and HIF-1α levels, and inhibiting p-ERK further reduced HIF-1α and VEGF.

Conclusions:

  • GIT1 plays a crucial oncogenic role in osteosarcoma.
  • GIT1 knockdown effectively inhibits osteosarcoma growth, invasion, and angiogenesis.
  • GIT1 represents a promising molecular target for osteosarcoma gene therapy.
Keywords:
ERK1/2GIT1HIF-1αangiogenesisorthotopic femoral osteosarcoma modelosteosarcoma

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