ArticleFrontiers in oncology2026
Lenvatinib induces ferroptosis-related changes in osteosarcoma cells involving the p-STAT3/p53/xCT axis.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Lenvatinib is an effective antitumor agent for several solid tumors and has been used in pediatric and adolescent patients with refractory or recurrent osteosarcoma. However, the mechanism by which lenvatinib suppresses osteosarcoma progression remains incompletely defined. This study investigated whether lenvatinib induces ferroptosis-related changes in osteosarcoma cells and explored its effects on malignant biological behavior and the underlying molecular mechanism. Methods: Human osteoblast hFOB1.19 cells and osteosarcoma MG63, 143B, and U2OS cells were treated with lenvatinib. Cell viability and IC50 values were determined using CCK-8 assays. Ferroptosis-related molecular changes in 143B and U2OS cells were evaluated by qRT-PCR, Western blotting, flow cytometry, and biochemical assays measuring intracellular Fe Results: Lenvatinib inhibited the proliferation of 143B and U2OS cells in a concentration-dependent manner, whereas its inhibitory effect was weaker in MG63 cells and limited in hFOB1.19 osteoblasts. Transmission electron microscopy revealed ferroptosis-associated mitochondrial alterations, including mitochondrial shrinkage, loss or reduction of cristae, and increased membrane density. Lenvatinib increased intracellular Fe Discussion: These findings suggest that lenvatinib suppresses osteosarcoma cell proliferation, migration, and invasion, at least in part, by inducing ferroptosis-related changes associated with modulation of the p-STAT3/p53/xCT axis. This study reveals a previously underrecognized mechanism of lenvatinib action and supports further investigation of ferroptosis-targeted strategies in osteosarcoma.
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