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Targeting RSK2 enhances the efficacy of IGF1R inhibitor against triple-negative breast cancer via antagonizing IGF1/IGF1R signaling mediated by GATA3-IGFBP5 pathway.

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Acta pharmacologica Sinica 📖 저널 OA 78% 2022: 1/1 OA 2025: 11/11 OA 2026: 27/38 OA 2022~2026 2026 Vol.47(5) p. 1300-1311 OA Growth Hormone and Insulin-like Grow
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PubMed DOI PMC OpenAlex 마지막 보강 2026-04-29
OpenAlex 토픽 · Growth Hormone and Insulin-like Growth Factors Metastasis and carcinoma case studies Cancer, Hypoxia, and Metabolism

Shan TJ, Li LY, Wan XY, Li YZ, Jiang T, Chen ZL

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Targeting the IGF1 system holds promise as a therapeutic approach for breast cancer.

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APA Tian-jiao Shan, Lei Li, et al. (2026). Targeting RSK2 enhances the efficacy of IGF1R inhibitor against triple-negative breast cancer via antagonizing IGF1/IGF1R signaling mediated by GATA3-IGFBP5 pathway.. Acta pharmacologica Sinica, 47(5), 1300-1311. https://doi.org/10.1038/s41401-025-01673-w
MLA Tian-jiao Shan, et al.. "Targeting RSK2 enhances the efficacy of IGF1R inhibitor against triple-negative breast cancer via antagonizing IGF1/IGF1R signaling mediated by GATA3-IGFBP5 pathway.." Acta pharmacologica Sinica, vol. 47, no. 5, 2026, pp. 1300-1311.
PMID 41501418 ↗

Abstract

Targeting the IGF1 system holds promise as a therapeutic approach for breast cancer. However, the intricate nature of IGF1 signaling and suboptimal drug combinations have resulted in limited clinical success. This study demonstrates that silencing p90 ribosomal S6 kinase 2 (RSK2), a downstream effector of the Ras/ERK pathway, inhibits IGF1 signaling by upregulating the expression and secretion of IGFBP5, a potent inhibitor of the IGF1-IGF1R axis that competes with IGF1 for binding. Mechanistically, GATA3 is identified as a novel transcription factor for IGFBP5, and RSK2 promotes GATA3 degradation by directly binding and phosphorylating it at serine 308, thus suppressing IGFBP5 transcription. Moreover, combined treatment with the RSK2 inhibitor LJH685 and the IGF1R inhibitor PPP significantly reduces metastasis of triple-negative breast cancer (TNBC) in both in vitro and in vivo models. These findings uncover new targets for synergistic antitumor therapy in TNBC and suggest that concurrent inhibition of IGF1R and RSK2 may offer an effective combinatorial treatment strategy.

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