IndraLab

Statements


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"It was also clarified that aberrant fatty acid metabolism (FAM) might accelerate tumor growth and metastasis of HCC."

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"Suppression of USP9X in OSCC has emerged as a potential strategy to inhibit tumor growth, suggesting that USP9X is a potential therapeutic target for this cancer type [97]."

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"FAM also contributes to therapy resistance, including resistance to chemotherapy, radiation therapy, and therapies targeting tumors with complex and diverse mechanisms (19)."

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"We observed that the FAM signal in the tumors correlated with the PEG5K-lipid density of the CLs."

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"Therefore, USP9X promotes the metastasis of tumor cells76."

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"The high expression of USP9X in OSCC cells increases the stability of PD-L1 in OSCC cells by deubiquitinating the tumor and promoting immune escape (95)."

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"This NDRG3-dependent tumor-promoting activity of USP9X in KRAS-driven pancreatic tumorigenesis might be specifically inhibited by targeting the KRAS-NDRG3-USP9X axis.NDRG3 protein was predicted to assume flexible structures at the N- and C-terminal regions, unlike the central NDR domain with an ordered structure consisting of α-helices and β-sheets (https://xtalpred.godziklab.org/XtalPred-cgi/xtal.pl) ."

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"USP9X Increased Tumor Angiogenesis in Mantle Cell Lymphoma by Upregulation of CCND1-Mediated SOX11."

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"USP9X also cooperates with the proto-oncogene Kras to promote pancreatic tumorigenesis in vivo by rapidly developing advanced pancreatic intraepithelial neoplasia and microinvasive neoplasms [157]."

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"Recent studies have shown that FAM can modulate the tumor immune microenvironment (72, 73), and enrichment analysis results indicate that genes within the high-risk cohort are primarily linked to immune pathways."

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"The measurements of the xenograft tumor size (Figure 4B) and weight (Figure 4C) demonstrated that the knockdown of USP9X or TTK suppressed tumor growth."

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"Compared to the control group, knockdown of USP9x markedly reduced the tumor size ( Fig. 8 B) and weight ( Fig. 8 C and D)."

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"Recent studies suggest that FAM may modulate tumor biological behavior by affecting the local TME (22)."

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"Moreover, knockdown of USP9X or TTK inhibited cell proliferation, migration and tumorigenesis, and the immunohistochemical analysis of clinical NSCLC samples showed that the protein expression levels of USP9X and TTK were significantly elevated and positively correlated in tumor tissues.Conclusions: In summary, our data demonstrated that the USP9X-TTK axis may play a critical role in NSCLC, and could be considered as a potential therapeutic target."

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"Using PANC-1 PC cell line, USP9X was reported to promote tumor metastasis and inhibit tumor apoptosis [ 34 ]."

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"USP9X promotes tumor development as well as chemoresistance in B-cell malignancies [ 52–54 ]."

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"WP1130, an inhibitor of USP9X, can prevents prostate tumor growth in vitro [46]."

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"Figure 7A and B shows that USP9X knockdown suppressed tumor volume and weight."

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"In the same study , it was observed that MCL-1 levels were increased in malignant tissues from melanoma patients while Beclin1 was destabilized , suggesting that USP9X promotes tumor progression ."

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"USP9X overexpression significantly increased xenograft tumor growth in the BALB/c mice compared with the control group (P<0.01) (Figure 5A, 5B)."

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"Studies related to other malignancies, such as pancreatic cancer, demonstrated that Usp9X is necessary to drive tumor growth by inhibition of cell death ."

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"USP9X gene knockout in the MCF-7 cells reduced the xenograft tumor growth compared with that of cells transfected with negative CRISPR/Cas9 vector (P<0.01)."

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"Downregulating USP9X increased tumor sensitivity to chemotherapy by degrading the MCL1 protein [31]."

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"OSCC cell tumor development can be dramatically reduced by USP9X knockdown.113 Therefore, targeting PD-L1 by blocking or silencing USP9X may provide an effective strategy in cancer immunotherapy."