IndraLab

Statements


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"Functionally, USP7 overexpression promoted cell growth and invasion via deubiquitination of EZH2."

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"Interestingly , USP7 inhibitor suppressed cell growth in both GSI-sensitive ( CUTLL1 ) and GSI-resistant ( JURKAT , MOLT-4 , and CCRF-CEM ) T-ALL cells , thus providing a rationale for inclusion of USP7 inhibitors in a GSI-based regimens for treatment of T-ALL patients ."

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"USP7 silencing in MEC-1 cells abrogated cell growth, corroborating the bona fide data we obtained with the inhibitor."

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"These experiments showed that USP7 haploinsufficiency decreases the E protein activity of E2A and HEB and promotes T-ALL cell growth."

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"USP7 haploinsufficiency promotes T-ALL cellular growth."

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"Since NOTCH1 plays a significant role in T-ALL pathogenesis, we proposed that loss of function of USP7, which deubiquitinates and stabilizes ICN1, might inhibit T-ALL cell growth."

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"Inhibitors of USP7 have been recently shown to suppress tumor cell growth in vitro and in vivo."

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"HAUSP strongly stabilizes p53 even in the presence of excess Mdm2, and also induces p53 dependent cell growth repression and apoptosis."

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"USP7 inhibition severely impaired the cell growth of MOLM-13, OCI-AML3, K562, and HL60 AML cell lines (Figure 8A)."

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"In particular, pharmaceutical inhibition of USP7 by the small molecule P22077 attenuated PDAC cell growth and induced cell death in vitro and in vivo."

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"We also show that USP7 and NOTCH1 bind T-ALL superenhancers, and inhibition of USP7 leads to a decrease of the transcriptional levels of NOTCH1 targets and significantly blocks T-ALL cell growth in vitro and in vivo."

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"Our finding that USP7 inhibition in vitro and in vivo significantly suppresses leukemic cell growth, alone and in combination with chemotherapy, independently of p53 status supports this notion."

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"In this study, we demonstrated that loss of USP7 function inhibits cell growth by promoting cell cycle arrest and apoptosis in A375 and B16 cells."