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RIP assay revealed that AWPPH could bind to EZH2 and ChIP assay showed SMAD4 was regulated by EZH2. LncRNA AWPPH can promote cell proliferation, autophagy, and migration, as well as inhibit cell apoptosis in bladder cancer by inhibiting SMAD4 via EZH2.
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Concluded that SMAD4 inhibits the H2O2-induced apoptosis in osteoblast hFOB1.19 cells; such inhibition might depend on the SUMOylation by SUMO 2/3. It implies a promising role of SMAD4 in oxidative stress-promoted damage to osteoblasts.
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Data show that miR-301a suppressed the expression of cyclin-dependent kinase inhibitor p21 (p21) and Smad4 protein, and subsequently promoted G1/S cell cycle transition and cell proliferation in vitro and xenograft growth in nude mice in vivo.
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miR-422a suppressed SMAD4 expression and inhibited TGF-beta and bone morphogenetic protein-dependent luciferase activity in muscle cells.
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as a direct target of miR-224, USP3 is a potent ceRNA of SMAD4 in CRC. Decreased expression of USP3 mRNA is associated with a poor prognosis and distal metastasis of CRC, which is attributed to further suppression of SMAD4 through the release of miR-224 from the USP3 3'UTR.
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We report a 2-year-old girl diagnosed with Myhre syndrome by whole exome sequencing (WES) that revealed the recurrent p.Ile500Val mutation in the SMAD4 gene
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ENG, ACVRL1, and SMAD4 mutations result in different phenotypes in hereditary hemorrhagic telangiectasia
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Our results demonstrated that SMAD4 and NF1 mutations can serve as potential biomarkers for poor prognosis to cetuximab-based therapy in Chinese mCRC patients.
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miRNA-34a suppressed the TGF-beta-induced epithelial mesenchymal transformation, invasion, and migration of nasopharyngeal carcinoma cells by directly targeting SMAD4.
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Overall, these findings suggest a more dominant role for SMAD3 and SMAD4 than SMAD2 in TGFbeta-induced chondrogenesis of human bone marrow-derived mesenchymal stem cells.
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miR-205 functions as an oncogenic miRNA by directly binding to SMAD4 and PTEN, providing a novel target for the molecular treatment of ovarian cancer.
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Smad4 deletion may inhibit lipogenesis, stimulate beta-oxidation, improve lipid metabolism and liver function, alleviate inflammation and fibrosis, and reduce cell apoptosis in nonalcoholic steatohepatitis.
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a constructed SMAD4 RNA interference experiment confirmed that the function of KCNQ1OT1 was to act on lens epithelial cell proliferation and EMT, and this was achieved via the SMAD4 signaling pathway. The findings of the present study may provide a novel target for molecular therapy of cataracts disease.
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Serum BMP2 and Smad4 levels in patients with senile osteoporotic fracture were significantly lower than those in normal controls
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The tumor suppressor gene SMAD4 (DPC4) may help predict which surgical patients are at higher risk for failure after definitive management and may benefit from intensified adjuvant therapy.
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Smad4 could be considered as a central component of EMT transition in human colorectal cancer that combines with transcriptional factors to reduce E-cadherin and alter the expression of the epithelial phenotype.
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LPS mediates intercellular tight junction destruction among TECs and RhoT1/SMAD-4/JAM-3 is a pivotal pathway to mediate the phenomenon.
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the results indicated that miR3147 may serve an oncogenic role in vulvar squamous cell carcinoma (VSCC) by targeting Smad4. miR3147 may represent a novel potential therapeutic target marker for VSCC.
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Data indicate that in pancreatic cancer cells, the expression of ENG may be controlled by a pathway mediated by SMAD4.
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Data indicate that absence of KRAS, TP53 and SMAD4 genetic alterations may identify a subset of pancreatic carcinomas with better outcome.
