Fig. 7: A schematic model of GASP1 promoting malignant phenotypes of breast cancer cells and decreasing their response to paclitaxel by forming a positive feedback loop with the IGF1/IGF1R pathway. | Cell Death & Disease

Fig. 7: A schematic model of GASP1 promoting malignant phenotypes of breast cancer cells and decreasing their response to paclitaxel by forming a positive feedback loop with the IGF1/IGF1R pathway.

From: GASP1 enhances malignant phenotypes of breast cancer cells and decreases their response to paclitaxel by forming a vicious cycle with IGF1/IGF1R signaling pathway

Fig. 7

In GASP1-deficient cells, IGF1R stability can be regulated by MDM2-mediated ubiquitination degradation. When GASP1 is overexpressed in breast cancer, GASP1 interacts with and stabilizes IGF1R by preventing the MDM2-mediated IGF1R ubiquitination degradation, thereby activating its downstream signaling pathways such as NF-κB, PI3K/AKT, and MAPK/ERK pathways. IGF1, in turn, stimulated GASP1 expression by activating the PI3K/AKT pathway, forming a vicious cycle propelling the malignant progression of breast cancer and decreasing the cellular response to paclitaxel in breast cancer.

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