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Fluoxetine Suppresses Osteosarcoma ProgressionIn Vivoby Inducing Apoptosis and Inhibiting the AKT/mTOR/NF-κB Signaling Pathway

Year: 2025

Type: article

Abstract: BACKGROUND/AIM: OSCC model. MATERIALS AND METHODS: Mice inoculated with U-2 OS cells were treated with fluoxetine (10 or 20 mg/kg) to evaluate tumor growth, metastasis, and underlying molecular mechanisms. RESULTS: Fluoxetine treatment resulted in a dose-dependent reduction in tumor volume and weight, without causing systemic toxicity, as confirmed by histopathological and biochemical analyses. Mechanistically, fluoxetine activated caspase-dependent apoptosis by up-regulating cleaved caspase-8, caspase-9, and caspase-3. It also inhibited OSCC metastasis by suppressing VEGF and MMP-9 expression, reducing epithelial-mesenchymal transition markers. Furthermore, fluoxetine significantly reduced the phosphorylation of AKT, PRAS40, mTOR, and NF-[Formula: see text]B, thereby disrupting key tumorigenic signaling pathways. CONCLUSION: Fluoxetine demonstrates promising anti-tumor activity in OSCC by inducing apoptosis, inhibiting metastasis, and targeting oncogenic signaling pathways. These findings suggest that fluoxetine may serve as a potential therapeutic agent for OSCC, warranting further investigation for clinical application.

Source: Anticancer Research

DOI: 10.21873/anticanres.17530

Authors: YU-HSI CHEN, CHI-HUAN LI, SHIH-WEI LIU, FEI-TING HSU, MING-CHOU KU

Institutions: Chang Bing Show Chwan Memorial Hospital, National Yang Ming Chiao Tung University, National Central University, Central Taiwan University of Science and Technology

Language: English

Topic: PI3K/AKT/mTOR signaling in cancer

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: hybrid

OpenAlex ID: W4408997623

FWCI: 0.761

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Cited by: 3

Related to: 10