THBS2 Promotes Prostate Cancer Malignancy via INHBA‐Dependent FAK/PI3K/AKT Signaling Activation
Year: 2026
Type: article
Abstract: Prostate cancer (PCa) is a leading malignancy among men, with a growing incidence and mortality rate worldwide. There is a pressing need to identify novel molecular biomarkers and therapeutic targets to improve prognosis and treatment strategies for PCa. We analyzed thrombospondin 2 (THBS2) expression patterns in PCa using The Cancer Genome Atlas (TCGA) datasets and validated findings in clinical tissues and cell lines. Functional assays, including Cell Counting Kit (CCK)-8 proliferation, flow cytometry apoptosis, wound healing, and Transwell invasion, were performed on PCa cell lines with altered THBS2 expression. Bioinformatic analyses were conducted to explore THBS2-related pathways, and protein interactions were examined via STRING and Western blot. THBS2 expression was significantly upregulated in PCa tissues and cell lines and correlated with advanced clinicopathological features and poor prognosis. Overexpression of THBS2 promoted PCa cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while inhibiting apoptosis. Mechanistically, THBS2 interacted with INHBA to activate the focal adhesion kinase (FAK)/PI3K/AKT signaling pathway, facilitating malignant progression. INHBA knockdown reversed the oncogenic effects of THBS2, indicating a synergistic interaction between THBS2 and INHBA in PCa pathogenesis. THBS2 acts as an oncogene in PCa by promoting proliferation, invasion, and EMT via the FAK/PI3K/AKT pathway in cooperation with INHBA. These findings highlight THBS2 as a promising biomarker for PCa.
Source: Analytical Cellular Pathology
DOI: 10.1155/ancp/3503659
Authors: Yifeng Yao, Yiyang Guo, Shoulei Liu, Yaojun Li, Shanmiao Chen
Institution: Hangzhou Medical College
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,160
OpenAlex ID: W7119789557