VEGF Silencing Inhibits Human Osteosarcoma Angiogenesis and Promotes Cell Apoptosis via PI3K/AKT Signaling Pathway.

Area of Science:

• Oncology
• Molecular Biology
• Biochemistry

Background:

• Vascular endothelial growth factor (VEGF) is a key promoter of tumor vasculature.
• VEGF is frequently upregulated in cancers like osteosarcoma and glioma.
• Understanding VEGF's role is crucial for developing anti-cancer therapies.

Purpose of the Study:

• To investigate the molecular mechanisms inhibiting tumor growth via VEGF expression interference.
• To assess the efficacy of VEGF silencing in osteosarcoma cells (U2OS).

Main Methods:

• Construction of a Lv-shVEGF vector for VEGF silencing.
• In vitro assessment of VEGF silencing efficiency on U2OS cell proliferation and apoptosis.
• In vivo evaluation of osteosarcoma tumor growth and angiogenesis.
• Analysis of PI3K/AKT signaling pathway activation.

Main Results:

• Lv-shVEGF demonstrated high efficiency in inhibiting VEGF expression.
• VEGF silencing suppressed U2OS cell proliferation and promoted apoptosis in vitro.
• Osteosarcoma tumor growth and angiogenesis were significantly reduced in vivo.
• Activation of the PI3K/AKT signaling pathway was decreased following Lv-shVEGF treatment.

Conclusions:

• VEGF silencing is a promising strategy for suppressing osteosarcoma progression.
• The mechanism involves reduced cell proliferation, enhanced apoptosis, and decreased angiogenesis.
• Inactivation of the PI3K/AKT signaling pathway mediates these anti-tumor effects.