THBS2 Promotes Prostate Cancer Malignancy via INHBA-Dependent FAK/PI3K/AKT Signaling Activation

Area of Science:

• Oncology
• Molecular Biology
• Biochemistry

Background:

• Prostate cancer (PCa) presents a significant global health challenge with increasing incidence and mortality.
• Novel molecular biomarkers and therapeutic targets are crucial for improving PCa prognosis and treatment.
• Thrombospondin 2 (THBS2) has emerged as a potential factor in cancer development.

Purpose of the Study:

• To investigate the role of thrombospondin 2 (THBS2) as a molecular biomarker and therapeutic target in prostate cancer (PCa).
• To elucidate the underlying mechanisms by which THBS2 influences PCa progression.

Main Methods:

• Analysis of THBS2 expression in The Cancer Genome Atlas (TCGA) datasets and clinical PCa tissues/cell lines.
• In vitro functional assays (proliferation, apoptosis, migration, invasion) in PCa cell lines with modulated THBS2 levels.
• Bioinformatic analysis of THBS2-related pathways and protein-protein interactions (STRING, Western blot).

Main Results:

• THBS2 expression is significantly upregulated in PCa tissues and cell lines, correlating with advanced features and poor prognosis.
• Overexpression of THBS2 enhances PCa cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while suppressing apoptosis.
• THBS2 interacts with INHBA, activating the FAK/PI3K/AKT pathway, thereby promoting PCa malignancy.

Conclusions:

• THBS2 functions as an oncogene in prostate cancer, driving proliferation, invasion, and EMT through the FAK/PI3K/AKT pathway in conjunction with INHBA.
• THBS2 represents a promising biomarker for prostate cancer diagnosis and a potential therapeutic target.