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USP7 activates Neoplasms. 65 / 66
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"As shown in Fig. 6 A , inhibition of USP7 dramatically decreased the tumor size of both C33A and MS751 cells compared to control groups."
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"These results further confirmed that inhibition of USP7 could efficiently suppress cervical tumor growth and metastasis in vivo.In previous studies of cervical cancer, it is found that USP7 is overexp[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"TRIM24 silencing also counteracted USP7 overexpression-mediated down-regulation of Ki67 and up-regulation of SPLUNC1 in tumors (Fig. 8D)."
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"USP7 mediates cell cycle control, tumor growth, chemoresistance, and tumor immunity by regulating multiple cellular signaling pathways, including the p53 and Wnt pathways (33, 34)."
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"USP7 promotes cell proliferation, migration, in vitro invasion, and tumor growth by stabilizing TAZ."
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"Inhibition of USP7 significantly suppresses tumor growth in HNSCC xenografts and PDX models (23)."
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"These findings have shown that USP7 may induce tumour progression and be a therapeutic target ."
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"These data revealed that USP7 inhibitor suppresses GC cell proliferation and cell cycle progression.3.4 USP7 knockdown suppressed GC tumor growth in vivo ."
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"USP7, one of the DUB genes, induces tumors by stabilizing HIF-1α."
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"As exhibited in Fig. 6A–C, USP7 knockdown suppressed tumor growth in vivo, reflected by smaller tumor volume and lighter tumor weight in sh-USP7 group, while MTDH overexpression reversed the anti-growth effect of sh-USP7."
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"USP7 selective inhibitors have been found to significantly repress the growth of multiple tumor xenograft models in immunodeficient mice, including multiple myeloma, B-cell leukemia and neuroblastoma (129)."
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"Based on our results, we confirmed the tumor-promoting function of Usp7 in breast cancer."
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"27 Targeting USP7 catalytic activity may also relieve inactivation of other tumor suppressors, such as FOXO4 and PTEN, and may have an overall beneficial effect as an anticancer therapeutic strategy."
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"To substantiate the pro-tumorigenic roles of USP7, we further exploited an HNSCC xenograft model and found that USP7 knockdown reduced tumor growth in vivo, accompanied by diminished TAZ and Ki-67 expression in samples (Fig. 2E–G)."
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"Inhibition of USP7 can effectively reverse ITME in subcutaneous tumor models of lung cancer."
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"Above results let us make a hypothesis that knockdown of USP7 can suppress GC tumor growth in vivo, the ability of USP7-knockdown cells to affect tumor growth was detected in xenograft model bearing Con and USP7 KD MKN45 cells."
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"USP7 promoted cell proliferation, migration, invasion in vitro and tumor growth by stabilizing TAZ."
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"The results in Figure 4A showed that knockdown of USP7 in MKN45 cells significantly reduced tumor size compared to the control group."
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"Pharmacological inhibition of USP7 significantly suppressed tumor growth in both xenograft and PDX models."
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"We investigated the expression and effects of USP7 in ERPBC and demonstrated that CDK1 levels are regulated by USP7, which promotes tumor progression in ERPBC."
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"USP7 knockdown significantly inhibited in vivo tumor growth in both PDXs and in two additional samples from affected individuals, MM25 (BRAF mutant) and MM16 (NRAS mutant) ( Figure 1 F), resulting in [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"However, a related study showed that inhibiting USP7 increased the expression of PD-L1 in lung cancer cells (Dai et al., 2020), and higher levels of USP7 promoted tumor growth by altering the immunosuppressive characteristics of Forkhead box protein P3 (Foxp3) Treg (Gao et al., 2023)."
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"In particular, compound 41, both highly potent and selective against USP7, is orally bioavailable and demonstrates tumor growth inhibition in both p53 wild type and p53 mutant cancer cell lines in xenograft studies , suggesting that the inhibition of USP7 could suppress tumor growth through multiple pathways, thereby delineating a possible clinical application."
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"Although numerous studies indicate that inhibition of USP7 suppresses tumor growth by activating p53, the precise mechanism by which USP7 contributes to tumor growth through the p53-independent manner is not well understood."
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"Conversely, USP7 knockdown destabilizes Foxp3 and decreases Treg cell-induced suppression in vitro and in vivo [69] , enabling immune-mediated tumor suppression [70] ."
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"Furthermore, research suggests that overexpression of USP7 in human tumors inhibited tumor cell cycle arrest and promoted apoptosis, thereby promoting tumor progression."
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"Targeting USP7 can enhance the tumor response to various therapeutic strategies, including traditional chemotherapy, molecular targeted therapy, immunotherapy, and radiotherapy."
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"Within tumor inflammation, USP7 modulates tumor growth and immune responses by removing ubiquitin tags from key proteins, thereby altering their stability and function [4]."
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"Together, our findings indicate that FOXM1 is a major target of USP7 in modulating tumor growth in a p53-independent manner and reveals the USP7 degrader as a potential therapeutic tool for the treatment of triple-negative breast cancers."
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"Our experiment proved that OBB downregulated the expression of USP7 mainly by inhibiting the NOTCH1 pathway.This study reported the tumor-inhibiting role of OBB, indicating that it may be used as a sensitizer for sorafenib in liver cancer."
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"Moreover , USP7 promotes tumor progression by deubiquitinating and stabilizing the histone demethylase PHF8 and by upregulating cyclin A2 in breast cancer ( Wang et al. 2016 ) ."
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"The subcutaneous stromal plug model in nude mice confirmed the role of SNAI2 in USP7-mediated tumor VM in vivo (Fig. 5P, Q)."
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"Inhibition of USP7 induces p53-independent tumor growth suppression in triple-negative breast cancers by destabilizing FOXM1."
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"USP7 was shown to deubiquitinate and stabilize the ERα subunit, promoting cell proliferation and tumor growth in ER-positive BC by inhibiting cell cycle arrest and apoptosis [35]."
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"A high USP7 expression may promote cancer progression and predict unfavourable prognosis of cancer patients , especially those with EOC ."
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"In vivo, disruption of Usp7 expression in SHH-MB blocks tumor proliferation."
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"Loss of USP7 or Raptor suppressed OS tumor growth in vivo."
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"Our findings showed that USP7 promotes tumor progression and metastasis of ERPBC via direct regulation of CDK1 stability."
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"USP7 inhibitors likewise inhibit tumor proliferation and promote PD-1 / PD-L1 expression and immune response ( 31 ) ."
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"For example, USP2 and USP7 modulate p53 and MDM2, impacting cell survival and tumor development, while USP22 stabilizes c-Myc, driving cancer proliferation and metastasis [9–13]."
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"USP7 exhibits a high expression signature in various malignant tumors, and increased USP7 expression often indicates the poor tumor prognosis, suggesting that USP7 is a marker of tumor prognosis and a potential drug target for anti-tumor therapy."
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"It is noteworthy that USP7i effectively suppress tumor growth in both TP53 wild-type and mutant cells, suggesting that USP7 inhibition can impede tumor growth through mechanisms that are reliant on and independent of p53 ."
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"Notably, overexpression of USP7 substantially rescued the cellular viability and tumor growth in the presence of cabozantinib (Fig. S6, E and F)."
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"We have demonstrated that high expression of USP7 is associated with poor prognosis in children with NB and with other biological features of poor prognosis such as MYCN amplification and increased tumor stage."
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"Here, we show in vivo that deletion of Usp7 in Apc-truncated mice inhibits crypt hyperproliferation and intestinal tumor development."
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"It has been reported that USP2a, USP7, USP21, and USP22 are highly expressed in the HCC tissue or cells and promote tumor development (Cai et al., 2015; Li et al., 2018; Ling et al., 2020; Xiong et al., 2021)."
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"The overexpression of USP7 leads to changes in DNA damage response, apoptosis and cell cycle, thus causing tumor progression."
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"Deubiquitinase USP7 stabilizes KDM5B and promotes tumor progression and cisplatin resistance in nasopharyngeal carcinoma through the ZBTB16/TOP2A axis."
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"Conversely, USP7 interacts with FAM188B and enhances tumor growth and survival of colon cancer cells[28,36]."
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"Comprehensive analyses of three different Apc-deletion mouse models show that loss of Usp7 significantly reduces crypt hyperproliferation, WNT activation, and tumor development in Apc-deficient intestine."
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"Importantly, USP7 promotes PDAC tumor growth in a glycolysis-dependent manner."
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"USP7 inhibition stabilizes Foxp3, reduces Treg immunosuppression, and enables immune-mediated tumor suppression."
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"Comparison of Apc and Apc Usp7 cKO mice showed that Usp7 deletion significantly reduced tumor numbers at 4 months of age (Figures 3A and 3B)."
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"The results indicate that Usp7 deficiency inhibits tumor progression in Apc mice."
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"This theory’s generality is also manifested in the fact that targeting USP7 can help enhance tumor response to multiple therapeutic strategies, including traditional chemotherapy, molecular targeted therapy, immunotherapy, and radiation therapy."
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"USP7 was also shown to promote cancer by stabilizing beta-catenin and inducing signaling regulating cell fate determination and migration via the Wnt pathway [ 107 ] ."
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"Further , we found that USP7 inhibitor inhibited tumor proliferation via promoting the stability of P53 in GC and arrested the cell cycle at G2-M phase ."
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"USP7 promotes PDAC tumor growth in a glycolysis-dependent manner."
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"STAT3 and USP7 are upregulated at both RNA and protein levels in response to EZH2 inhibition.To address the questions that if there is resistance mechanism by which DLBCL cells tolerate EZH2 inhibitor treatment, we used EPZ to treat KARPAS-422 cells for 3 days and examined 11 oncogenic genes MYC, MAX, STAT3, KRAS, BCL2, BRAF, SRC, JUN, RAF1, SKI, FOS, MDM2, and a tumor suppression factor p53."
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"Altogether, these results indicate that inhibition of Usp7 suppresses intestinal tumor development and progression mediated by Apc-truncating mutations."
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"The results indicated that overexpression of SNAI2 significantly promoted tumor growth, while knockdown of USP7 markedly inhibited tumor growth."
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"These results are in concordance with the in vivo mouse data that USP7 inhibition suppresses hyperproliferation and tumor development specifically in APC-deficient intestine.Next, we explored if USP7 inhibition could be used as an adjuvant therapy to fluorouracil (5-FU), a common chemotherapy given to patients with CRC in the clinic."
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"Inhibition of USP7 reduces oncogene function, augments tumor suppression, and sensitizes tumors to DNA damaging agents."
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"Loss of Usp7 significantly reduces tumor numbers and tumor grade in both models, indicating that Apc-deficient tumor development and progression is Usp7 dependent."
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"In addition, USP7 enhanced tumor-promoting M2 polarization by inhibiting the M1 polarization of macrophages.Our study further expanded the role of USP7, showing that it not only inhibits tumor cell death through deubiquitination mechanisms but also promotes tumor progression by regulating the immune microenvironment."
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