IndraLab

Statements



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"USP8 also promotes epithelial-mesenchymal transition (EMT), invasion, and metastasis of tumor cells in response to TGF-β/SMAD signaling."

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"Knockdown of USP8 inhibits prostate cancer cell growth , proliferation , and metastasis and promotes docetaxel 's activity by suppressing the NF-kB signaling pathway Ubiquitin-specific protease 8 ( USP8 ) has been recently reported to be involved in tumorigenesis ."

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"Notably, accumulating evidence suggests that upregulated or mutated USP8 can lead to cancer progression, metastasis, and poor survival by affecting multiple signaling pathways in different types of tumors, including, but not limited to, lung [19], gastric [20], and breast cancers [21, 22]."

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"USP8 promotes the metastasis and its therapeutic advantage suppresses the metastatic activity 35811497."

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"USP8 promotes TGF-β/SMAD-induced EMT, invasion, metastasis, and facilitates TβRII circulating EVs to induce TEX and chemoimmunotherapy resistance (92)."

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"USP8 promotes TGF-β/SMAD-induced epithelial-mesenchymal transition (EMT), invasion, and metastasis in tumor cells."

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"In multiple studies (29–32), the EGFR is a substrate of USP8 deubiquitination, while USP8 has been shown to enhance gastric cancer cell proliferation and metastasis via the PI3K/AKT signaling pathway (30)."

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"Moreover, USP8 inhibition reduced epithelial-to-mesenchymal transition and reduced metastasis, according to western blotting analysis (Fig. S2e, f)."

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"As USP8 silencing significantly inhibited the PCa cell growth, proliferation, and metastasis and induced apoptosis and suppressed NF-kB signal activation by decreasing EGFR and PI3K, the USP8-specific inhibitor might be a novel therapeutic target to suppress PCa cell growth, proliferation, and metastasis."

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"Knockdown of USP8 inhibits prostate cancer cell growth, proliferation, and metastasis and promotes docetaxel's activity by suppressing the NF-kB signaling pathway."

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"31 For example, USP8 promoted breast cancer cell EMT and metastasis by deubiquitinating TGF‐β receptor TβRII."

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"Here , we find that the ubiquitin-specific protease 8 ( Usp8 ) promotes tumor cell migration through activating the c-Jun N-terminal kinase ( JNK ) pathway ."

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"In vivo xenograft and metastasis experiments indicate that inhibition of USP8 suppresses tumor growth and lung metastasis."

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"Usp8 promotes tumor cell migration through activating the JNK pathway ."

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"USP8 also promotes tumor metastasis, invasion, and epithelial‐mesenchymal transition in response to TGF‐β/SMAD signaling."

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"So, it can be assumed that the inhibition or silencing of USP8 may prevent the growth of GC cells as well as metastasis through the inhibition of this PI3K/AKT signaling pathway which is needed to pro[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"USP8 regulates NF-kappaB activation through EGFR and PI3K stabilization to promote PCa cell proliferation and survival In multiple studies ( 29-32 ) , the EGFR is a substrate of USP8 deubiquitination , while USP8 has been shown to enhance gastric cancer cell proliferation and metastasis via the PI3K / AKT signaling pathway ( 30 ) ."

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"In vivo using xenograft and tail vein injection mouse models indicated that inhibition of USP8 significantly reduced tumor growth and inhibited lung metastasis."