Preclinical study reveals that IGF2 knockout impairs proliferation and tumor growth in osteosarcoma models, indicating IGF2 promotes expansion without being strictly essential for survival.
Insulin-like growth factor 2 (IGF2) is implicated in osteosarcoma, but direct functional evidence of its role is lacking. Here, we used CRISPR-Cas9 to knock out IGF2 in Saos2 osteosarcoma cells. Knockout cells showed reduced proliferation in vitro which was fully restored by exogenous IGF2. In vivo, knockout xenografts reached only ~25% of wild-type tumor volume. Furthermore, transcriptomic analysis revealed depletion of angiogenesis-related genes but no major changes in IGF2 pathway components. Finally, while integration with receptor dependency data suggested alternative signaling pathways, IGF2 loss remained functionally limiting. These findings demonstrate that IGF2 promotes osteosarcoma proliferation and tumor growth but is not strictly essential for survival.
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Yao et al. (2026) studied this question.
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