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USP8 activates RTK. 9 / 9
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"ubiquitin-specific protease 8 (USP8) could enhance the stability of receptor tyrosine kinases (RTKs) such as EGFR and MET via deubiquitination, contributing to the proliferation ability of many human [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Thus, the knockdown of USP8 significantly reduced the downstream targets of RTKs including STAT3, Akt, and ERKs both as a phosphorylated and unphosphorylated form in gefitinib-resistant and -sensitive[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In addition, several RTKs including EGFR, HER-3, HER-2 were found to be decreased by USP8 knockdown [ 24 ], but the effects of USP8 on HER-3 in gastric cancer remained unclear till last year.Very rece[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"USP8 can also promote RTK stability (Berlin et al., 2010b; Mizuno et al., 2005; Niendorf et al., 2007)."

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"In addition, studies have shown that USP8 knockdown or inhibitors can significantly reduce the viability of gefitinib-resistant and -sensitive NSCLC cells by reducing the expression of receptor tyrosine kinase (RTK).14,15Baykara et al find that the serum USP8 level in NSCLC patients was higher than in healthy individuals."

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"An analysis of survival-related features of the cisplatin-resistant IGROV-1/Pt1 cells upon USP8 molecular targeting, indicated that USP8 interplays with RTKs since its silencing resulted in reduced activation of all RTKs belonging to the Human Epidermal Growth Factor Receptor (HER) family i.e., ErbB1/EGF-R, ErbB2, ErbB3 and ErbB4, and as a consequence decreased Akt activation as shown by reduced phosphorylation at Ser473."

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"Our findings are in keeping with the latter report and the view that reduced USP8 level may decrease activation of RTKs and as a consequence of the downstream PI3K/Akt pathway.Molecular targeting of USP8 revealed a link between FLIP and USP8, with down-regulation of FLIP upon USP8 silencing resulting in enhanced susceptibility to cisplatin-induced apoptosis as observed by Annexin V-binding assays in USP8-silenced cells."

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"The USP8 mediated stabilization of these RTKs activating STAT3, ERK, and pAKt downstream signaling pathways leading to promote cancer cell proliferation, survival, and metastasis [ 24 , 68 ]."

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"Furthermore, USP8 inhibition reduced levels of multiple receptor tyrosine kinases (RTKs) such as epidermal growth factor receptor (EGFR), and tyrosine‐protein kinase Met (c‐MET) up to 90%."