IndraLab

Statements

Mutated USP8 activates EGFR. 7 / 7
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"We found that USP8 mutated PAs have a higher incidence of EGFR expression, increased EGFR protein abundance and activation of downstream Erk1/2, indicating that USP8 mutations enhance EGFR signaling in tumors."
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"USP8 mutations, detected in up to two-thirds of Cushing disease, may underlie the increase in EGFR signalling in these tumours."
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"The USP8 mutation (14-3-3 somatic mutations) induces corticotroph EGFR adenoma signaling by rescuing EGFR from lysosomal degradation and enhancing EGFR accumulation (9)."
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"Previous studies have demonstrated that the USP8 mutation causes corticotroph adenomas mainly through activating the EGFR–MAPK signal cascades ."
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"In human corticotroph primary cultures, treatment with the pan-ErbB TKI canertinib as well as the EGFR TKI gefitinib suppresses POMC mRNA, and USP8 mutations, detected in up to two-thirds of CD, may underlie the increase in EGFR signaling in these tumors."
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"The USP8 mutation (14-3-3 somatic mutations) inhibits EGFR degradation, enhances EGFR accumulation, and consequently, likely induces corticotroph EGFR tumor signaling."
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"Considering that activation of EGFR-MAPK signaling induces p27 (Kip1) degradation, and p27 (Kip1)-deficient mice develop corticotropinoma XREF_BIBR, XREF_BIBR, we speculate that through activating EGFR signaling USP8 mutation accelerates p27 (Kip1) degradation, representing an important molecular mechanism underlying ACTH hyperproduction (XREF_FIG)."
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