IndraLab

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USP8 activates FGFR2. 4 / 4
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"Further inhibition of USP8 may more readily promote the degradation of FGFR2 via the proteasome."
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"The results of this study suggest that inhibiting USP8 promotes the degradation of FGFR2 via the proteasome, leading to suppression of STAT3 signaling in ARID1A-deficient OCCCs and subsequent induction of apoptosis.Since approximately half of OCCCs carry ARID1A-deficient mutations, synthetic lethal therapy using the USP8 inhibitors identified in this study could become a crucial personalized treatment approach."
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"Then, suppression of USP8 explicitly promotes the degradation of FGFR2 in ARID1A-deficient cells, and the STAT3 pathway, which is its downstream pathway, was suppressed, resulting in synthetic lethality by induction of apoptosis.ARID1A-deficient cancers include a significant number of gastric cancers, biliary tract cancers, and pancreatic cancers ."
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"Thus, our results suggest that inhibiting USP8 in ARID1A-deficient cells induces degradation of FGFR2, which in turn suppresses downstream STAT3 signaling and triggers apoptosis (Fig. 5H)."
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