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BTG2 Inhibits the Growth and Spread of Cervical Squamous Cell Carcinoma

John Logie Baird, Joseph Banks

Cervical squamous cell carcinoma (CSCC) is a prevalent form of cervical cancer characterized by uncontrolled growth and metastasis. Identifying novel therapeutic targets that can effectively suppress the progression of CSCC is crucial for improving patient outcomes. This study investigates the role of BTG2 (B-cell translocation gene 2) in the growth and spread of CSCC. We demonstrate that BTG2 expression is significantly downregulated in CSCC tissues compared to adjacent normal tissues. Using in vitro cell culture models, we show that BTG2 overexpression inhibits CSCC cell proliferation, induces cell cycle arrest, and promotes apoptosis. Moreover, BTG2 overexpression suppresses the migration and invasion capabilities of CSCC cells, as assessed by transwell assays. Mechanistically, we find that BTG2 modulates multiple signaling pathways involved in CSCC progression. Specifically, BTG2 inhibits the activation of the PI3K/Akt pathway, which is known to promote cell survival and migration. Furthermore, BTG2 upregulation leads to the downregulation of matrix metalloproteinases (MMPs), key enzymes implicated in extracellular matrix remodeling and cancer cell invasion. In a xenograft mouse model, we observe that BTG2 overexpression significantly reduces tumor growth and metastasis. Histological analysis reveals decreased proliferation and increased apoptosis in BTG2-overexpressing tumors compared to control tumors. Notably, BTG2 expression correlates with improved overall survival in a cohort of CSCC patients, highlighting its potential clinical relevance. Taken together, our findings demonstrate that BTG2 functions as a tumor suppressor in CSCC by inhibiting cell proliferation, migration, and invasion. These results suggest that targeting BTG2 could be a promising therapeutic strategy for the treatment of cervical squamous cell carcinoma. Further investigations are warranted to fully elucidate the underlying molecular mechanisms and to develop BTG2-based therapeutic approaches for clinical applications.