IndraLab

Statements


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"These results indicate that USP8 inhibition increases the sensitivity of cancer cells to ferroptosis in multiple cancer cell lines."

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"In the present study, we observed that inhibition of USP8 promoted ferroptosis of HCC cells."

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"Further analysis demonstrated that pharmacological inhibition or knockout of USP8 in HCC cells triggered ferroptosis and inhibited tumor growth both in vitro and in vivo."

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"Together, our study elucidates the physiological role of USP8 in suppressing extensive lipid peroxidation and ferroptosis via stabilizing GPX4 and highlights targeting the USP8-GPX4 axis as a potential strategy to enhance the efficacy of anti-PD-1 immunotherapy."

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"Collectively, this study demonstrates that pharmacological inhibition or knockout of USP8 can inhibit the progression of HCC and induce ferroptosis via decreasing the stability of OGT, which imposes a great challenge that targeting of USP8 is a potential approach for HCC treatment."

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"High expression of USP8 promoted the progression and inhibited ferroptosis of HCC ."

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"Professor Li and his team found that USP8 antagonized ferroptosis by stabilizing GPX4 in tumor cells and indicated that targeting USP8 may serve as a potential therapeutic strategy to promote ferroptosis to enhance cancer immunotherapy [96]."

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"Taking all these data into consideration, we conclude that SQSTM1 acts as a platform, tethering NCOA4 to LC3 during the process of ferritinophagy.In summary, we report that USP8 inhibition promotes ferroptosis by promoting ferritin degradation in cancer cells."

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"The ubiquitin specific peptidase 8 (USP8), which was found to favor HCC progression, inhibited the O-GlcNAcylation of SLC7A11 to stabilize its expression, thus facilitating the ferroptosis of HCC [26, 27]."

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"Overexpression of USP8 inhibits inflammation and ferroptosis in chronic obstructive pulmonary disease by regulating the OTUB1/SLC7A11 signaling pathway."

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"One previous study also suggested that the pharmacological inhibition of USP8 can induce ferroptosis and inhibit the progression of hepatocellular carcinoma by decreasing the stability of the O-GlcNAcylation of solute carrier family 7 member 11 (SLC7A11) [18]."

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"Targeting USP8 Inhibits O-GlcNAcylation of SLC7A11 to Promote Ferroptosis of Hepatocellular Carcinoma via Stabilization of OGT."

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"As shown in Fig. 6, inhibition of USP8 by DUB-IN-3 caused a dose-dependent suppression on the proliferation, invasion, stem-like properties and promoted ferroptosis of HCC cells (Fig. 6A–J)."

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"High expression of USP8 promoted the progression and inhibited ferroptosis of HCC."

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"In addition, overexpression of USP8 repressed ferroptosis by regulating glutathione peroxidase 4 and acyl-CoA synthetase long-chain family 4 expressions in COPD mice."

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"Furthermore, overexpression of USP8 suppressed ferroptosis in COPD cell model."