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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.
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the present study demonstrated the expression and clinical roles of miR-140 in glioma and suggested that miR-140 inhibited proliferation, migration and invasion of glioma cells, partially at least via suppressing ADAM9 expression. Therefore, miR-140 may be a novel candidate target for the development of therapeutic strategies for patients with glioma
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Increased ADAM9 mRNA expression is associated with esophageal adenocarcinoma.
