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USP8 inhibits apoptotic process. 23 / 24
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"These results demonstrated that knockdown of USP8 promoted cell apoptosis of lung cancer cells by regulating the PI3K/AKT pathway."
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"USP8 knockdown markedly induced apoptosis and cell cycle arrest ( G 0 / G 1 ) ."
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"USP8 knockdown markedly induced apoptosis and cell cycle arrest ( G 0/ G 1)."
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"Moreover, silencing of USP8 also promoted apoptosis in cholangiocarcinoma cells by regulating the Bcl-2 and Bax axis and Caspase cascade; up-regulation of USP8 decreased apoptosis in Hucct-1 cells."
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"In the present study , our objective is to study in broad the secondary down-stream effect after depleting USP5 or USP8 , which were initially showed to induce apoptosis in various cancers ."
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"DUB-IN-1 , an USP8 inhibitor , caused DNA damage , led to G2 / M phase block by p53-p21 axis , and triggered apoptosis by regulating the p53 target proteins including Bax , Noxa , and Puma ."
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"USP8 inhibitor , DUB-IN-1 , treatment could inhibit esophageal squamous cell carcinoma cell growth and induce G2 / M cell cycle arrest , apoptosis , and autophagy by DNA damage-induced p53 activation ."
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"Depletion of USP8 destabilized cFLIP resulting in sensitization to DR-induced apoptosis."
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"Knockdown of USP8 inhibited the proliferation of human lung cancer cells by regulating cell cycle- and apoptosis related proteins."
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"After transfection with siRNA1 or siRNA2, the expression of Bcl2 was reduced, while the expression of Bax was increased significantly both in A549 and H1299 cells (Figure 4B), indicating that knockdown of USP8 can induce apoptosis of lung cancer cells."
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"The data showed that knockdown of USP8 inhibited the proliferation and promoted the apoptosis of lung cancer cells."
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"High expression of USP8 can therefore inhibit extrinsic apoptosis by stabilizing FLIP L [ xref ] ."
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"Consistently, knockdown of USP8 significantly increased apoptosis of PIK3CA mutant cells even in the presence of glutamine (XREF_SUPPLEMENTARY)."
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"Taken together, our data indicate that USP8 functions as a novel deubiquitylase of FLIP L and inhibits extrinsic apoptosis by stabilizing FLIP L."
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"Knockdown of USP8 Promotes the Apoptosis of Lung Cancer Cells."
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"USP8 DUB prevents c-FLIP L, degradation and further halts the apoptosis in cancer cells suggesting it to be a potential drug target."
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"High expression of USP8 can therefore inhibit extrinsic apoptosis by stabilizing FLIP L [XREF_BIBR]."
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"USP8 inhibition via genetic and pharmacological approaches resulted in growth inhibition and apoptosis induction in both sensitive and doxorubicin resistant HCC cells."
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"Knockdown of USP8 inhibited the proliferation , migration , invasion , and cell cycle progression of A549 and H1299 cells , and promoted the apoptosis ."
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"Knockdown of USP8 increases apoptosis and enhances docetaxel-mediated apoptosis in PCa where its overexpression shows the opposite effects ."
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"Knockdown of USP8 inhibited the proliferation, migration, invasion, and cell cycle progression of A549 and H1299 cells, and promoted the apoptosis."
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"The silencing USP8 and docetaxel treatment reduced cell viability and migration and promoted apoptosis."
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"This study also shows that USP8 overexpression promotes PCa cell growth, survival, and migration and suppresses apoptosis."
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