High APEX1 Expression Facilitates Osteosarcoma Cell Proliferation.

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Osteosarcoma (OS) shows limited survival improvement over decades.
• Molecular targeted therapy presents a promising avenue for OS treatment.
• The role of Apurinic/apyrimidinic exonuclease 1 (APEX1) in OS proliferation is not fully understood.

Purpose of the Study:

• To investigate the expression of APEX1 in OS.
• To elucidate the mechanism by which APEX1 influences OS cell proliferation and apoptosis.
• To identify potential regulators of APEX1 in OS.

Main Methods:

• Real-time quantitative PCR (RT-qPCR) for gene expression analysis.
• Lentiviral vectors (APEX1-shRNA) for gene knockdown in MG-63 cells.
• MTT, xenograft tumor growth, and TUNEL assays for proliferation and apoptosis assessment.
• Bioinformatics analyses including PPI networks and pathway enrichment.

Main Results:

• APEX1 expression was significantly higher in OS tissues and cell lines compared to normal tissues and cells.
• APEX1 knockdown suppressed OS cell proliferation in vitro and in vivo, inducing apoptosis.
• APEX1 knockdown downregulated CD31 expression but did not affect P53 or Caspase3.
• Bioinformatics suggested USF1 or SP1 as potential regulators of APEX1 transcription.

Conclusions:

• Elevated APEX1 expression promotes OS cell proliferation, potentially via CD31.
• APEX1 knockdown inhibits OS progression and induces apoptosis.
• USF1 or SP1 may regulate APEX1 transcription and its role in DNA damage response pathways in OS.