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our results showed that ADAM9 is an important mediator of IL-6-induced hepatocellular carcinoma cell migration and invasion
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ADAM9 knock-out cells failed to produce viral progeny when incubated with encephalomyocarditis virus. However, bypassing encephalomyocarditis virus entry into cells through delivery of viral RNA directly to the cytosol yielded infectious virions from ADAM9 knock-out cells, suggesting that ADAM9 is not required for encephalomyocarditis virus replication post-entry.
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ADAM9 regulates beta1 integrin endocytosis. Reduced migration of ADAM9-silenced cells is, at least in part, caused by the accumulation and altered activity of beta1 integrin at the cell surface
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SNX9 knockdown revealed a nonredundant effect on overall ADAM9 protein levels, resulting in increased ADAM9 levels at the cell surface
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miR-129-5p suppressed cell proliferation and invasion ability through regulating ADAM9.
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Studies indicate that a disintegrin and a metalloprotease 9 (ADAM9) is involved in solid cancers with the different mechanisms which it employ to drive tumor progression [Review].
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Collective results suggested that galangin may act as an effective chemotherapeutic agent for glioma cancer depending on its ability to bring about ADAM9 and Erk1/2 activation.
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miR-543 serves as a tumor suppressor in glioblastoma multiforme through ADAM9 regulation.
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Study demonstrates that diabetes-mediated decrease in miR-126 leads to a corresponding increase in its target, ADAM9, which in turn cleaves MERTK (inactivates downstream engulfment signaling), thus resulting in defective macrophage efferocytosis of apoptotic cardiomyocytes.
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These results revealed that ADAM9 down-regulates miR-1 via activating EGFR signaling pathways, which in turn enhances CDCP1 expression to promote lung cancer progression.
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These findings suggested that miR302a inhibited osteosarcoma cell growth and metastasis by targeting ADAM9.
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Data show that ADAM9 is over-expressed in an activated form in human ovarian clear cell carcinomas, and suggest that it plays a key role in cisplatin resistance.
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Mechanistic investigations found that quercetin suppressed Snail-dependent Akt activation by upregulating maspin and Snail-independent a disintegrin and metalloproteinase (ADAM) 9 expression pathways to modulate the invasive ability of NSCLC cells
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ADAM9 is a component of cell-cell junctions. ADAM9 must be expressed by both adjacent cells for cell junction localisation. ADAM9 can self-associate via its ectodomain. The soluble ADAM9 ectodomain inhibits monocyte-endothelial transmigration.
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hese results emphasize the critical influence of ADAM9 on lung cancer progression and aggressiveness. ADAM9 should at least be a marker of cancer aggressiveness and a potential therapeutic target for cancer treatment.
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MiR-126-ADAM9 pathway-based therapeutic targeting may represent a novel approach for the inhibition of hepatitis B virus-related hepatocellular carcinoma metastases.
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miR-520f inhibited tumor cell invasion by directly targeting ADAM9 and the TGFbeta receptor TGFBR2.
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The results suggest that ADAM9 mRNA expression is associated with tumor grade and histological type in gliomas and can serve as an independent prognostic factor, specifically in LGG patients.
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ADAM9 could possibly be regarded as a biomarker for GC diagnosis and prevention. Moreover, as directly targeted by miR-126 in GC, ADAM9 may be a potential target for GC therapeutic treatment which warrants intensive study
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ADAM9 is a direct target of miR-20b and that miR-20b decreased the 5-FU resistance of HCT116-R cells.
