IndraLab

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TNFAIP3 inhibits cell population proliferation. 21 / 21
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"However, there are no reports on whether A20 can inhibit vascular smooth muscle cell proliferation in vivo."
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"The phenotype of this patient characterized by autoinflammation might be explained by increased cell proliferation and cell death caused by reduced TNFAIP3 (A20) expression."
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"A20 inhibits cell proliferation and migration by downregulating glucose metabolism ."
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"TNFAIP3 overexpression strongly inhibited CRC proliferation, invasion, and migration."
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"Here, we report that miR-125b is upregulated, whereas A20 is downregulated in NPC tissues relative to normal nasopharyngeal mucosa (NNM); miR-125b promotes NPC cell proliferation and inhibits NPC cell apoptosis by targeting A20/NF-κB signaling pathway; A20 inhibits NPC cell proliferation, induces NPC cell apoptosis, and reduces the growth of NPC xenograft tumors."
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"Results demonstrated that TNFAIP3 knockdown contributed to the proliferation, migration, invasion, and inflammation and suppressed the apoptosis in HAND2-AS1-overexpressed MH7A cells."
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"Importantly, TNFAIP3 knockout not only inhibited the AP20187 induced proliferation and tumor growth of DCIS-iFGFR1 cells, but also further reduced baseline proliferation and tumor growth of DCIS-iFGFR1 cells without AP20187 treatment."
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"Subsequent analysis has revealed that not only does A20 inhibits cell proliferation, but it has also been linked to the increased angiogenesis [ xref , xref ]."
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"Like CYLD , A20 suppresses cell proliferation and promotes apoptosis as a negative regulator of the NF-kappaB pathway , and it is well known to play an important role in inflammation and immunity ( Dixit et al. 1990 ; Hoesel and Schmid 2013 ) ."
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"A20 knockdown enhanced cell proliferation , clone formation , and migration , while A20 overexpression suppressed these capacities in HCC cells , both in vitro and in vivo ( Fig. 1a-d and Supplementary Fig. S1b ) ."
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"Furthermore, we revealed that TNFAIP3 overexpression inhibited CRC cell proliferation, invasion, and migration."
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"In addition, TNFAIP3 re-expression can inhibit proliferation, decrease expression of target genes in NF-kappaB signaling pathway, increase cytotoxicity and induce apoptosis in cells lacking TNFAIP3."
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"A20 Like CYLD , A20 suppresses cell proliferation and promotes apoptosis as a negative regulator of the NF-kappaB pathway , and it is well known to play an important role in inflammation and immunity ( Dixit et al. 1990 ; Hoesel and Schmid 2013 ) ."
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"With a combination of loss-of-function and gain-of-function approaches, we further showed that A20 inhibited NPC cell proliferation, induced NPC cell apoptosis, and reduced the growth of NPC xenograft tumors."
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"A20 inhibits SMC proliferation via increased expression of cyclin-dependent kinase inhibitors p21waf1 and p27kip1."
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"Furthermore, KO of TNFAIP3 inhibited cell proliferation when compared with their parent control cells in the absence of AP20187 treatment, suggesting that TNFAIP3 may also be required for the endogenous FGFR1-mediated cell growth or involved in other cell growth pathways."
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"A20 could also promote liver regeneration [ xref ] and inhibit HCC proliferation, metastasis and microvascular invasions [ xref , xref ]."
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"A20 inhibits cell proliferation and migration by downregulating glucose metabolism Aerobic glycolysis promotes tumor cell proliferation and migration ."
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"In summary, our data demonstrate that miR-125b is frequently upregulated in the NPC biopsies, and is an independent predictor for NPC patient survival; miR-125b regulates NPC cell proliferation and apoptosis by targeting A20/NF- κ B signaling pathway; A20 inhibits NPC cell proliferation and induces NPC cell apoptosis both in vitro and growth i n vivo ."
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"A20 Inhibited Proliferation, Migration, and Lipopolysaccharide-Induced Inflammation of SMCs via Increasing PPARα Expression."
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"In summary, we identified that SFE inactivated the NFkappaB pathway and down-regulated TNFAIP3 and PLAU expression to suppress ESCC cell proliferation and metastasis, providing new insights into the anticarcinogenic activity of SFE and confirming SFE as a potential chemotherapeutic agent."
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