IndraLab

Statements



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

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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 in this study, we found that knocking down USP8 significantly inhibited the PCa cell migration by suppressing the EMT process through the increased E-cadherin and decreased N-cadherin, whereas USP8 overexpression promoted the EMT process through the decreased E-cadherin and increased N-cadherin and so thereby increased the migration of both DU145 and PC3 cells.Knocking down USP8 downregulated the NF-κB signal by decreasing its intermediatory proteins (IKK, P-IKB, p65, and P-p65), whereas USP8 overexpression promoted the NF-κB signal by increasing its intermediatory proteins."

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"The results show that USP8 can promote the epithelial-to-mesenchymal transition (EMT) process by decreasing E-cadherin and increasing N-cadherin, thereby increasing the PCa cell migration and metastasis."