|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Treatment with AA and NG greatly inhibited Smad3 translation and phosphorylation while it restored Smad7 expression, and, therefore, it largely promoted NK cell differentiation, maturation, and cytotoxicity against cancer via Id2/IRF2-associated mechanisms.
|
30017880 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The transforming growth factor β1 (TGF-β1)/SMAD family member 3 (SMAD3) pathway, and hypoxia-inducible factor 1α (HIF-1α) are two key players in various types of malignancies including breast cancer.
|
30275854 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we used genetic engineering to generate a stable SMAD3-silencing human NK cell line, NK-92-S3KD, whose cancer-killing activity and cytokine production were significantly enhanced under TGFβ1-rich condition compared with the parental cell line.
|
29915022 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Smad3 linker phosphorylation is a candidate target for several kinases that play important roles in cancer cell initiation, proliferation and progression.
|
29097203 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Two miRNAs, hsa-miR-17-5p and hsa-miR-16-5p, were identified as having the highest associations with targeted mRNAs [such as B-cell lymphoma 2 (BCL2), small body size/mothers against decapentaplegic 3 (SMAD3) and suppressor of cytokine signaling 1 (SOCS1)] and pathways associated with epithelial-mesenchymal transitions and other processes linked with cancer metastasis (including cell cycle, adherence junctions and extracellular matrix-receptor interaction). mRNAs for two genes [HECT, UBA and WWE domain containing 1 (HUWE1) and BCL2] were found to have the highest associations with miRNAs, which were down-regulated in brain metastasis specimens of breast cancer.
|
28739740 |
2017 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Our findings represent a novel immunosuppressive function of TGFβ and demonstrate that TGFβ1 allows tumors to evade host immune responses in part through enhanced SMAD3-mediated PD-1 expression on TILs.Cancer Discov; 6(12); 1366-81.
|
27683557 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The TGFβ-SMAD3 pathway inhibits IL-1α induced interactions between human pancreatic stellate cells and pancreatic carcinoma cells and restricts cancer cell migration.
|
27473228 |
2016 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Therefore, we propose that loss of CTCF-dependent imprinting of tumor-promoting genes, such as IGF2 and TERT, results from a defective TGF-β pathway and is responsible at least in part for BWS-associated tumorigenesis as well as sporadic human cancers that are frequently associated with SPTBN1 and SMAD3 mutations.
|
26784546 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We report here that TGF-β directly regulates alternative splicing of cancer stem cell marker CD44 through a phosphorylated T179 of SMAD3-mediated interaction with RNA-binding protein PCBP1.
|
27746021 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
On the other hand, multiple important HCV viral proteins including CORE, NS3 and NS5A were found to target very important cancer related proteins such as TP53 and SMAD3, but no direct targeting to major immune response or inflammation related proteins.
|
23774196 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We show that mutation of the Smad3 linker phosphorylation sites greatly intensifies all TGFβ-induced responses, including growth arrest, apoptosis, reduction in the size of putative cancer stem cell population, epithelial-mesenchymal transition, and invasive activity.
|
25205100 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data suggest that TGFβ-dependent phosphorylation of 14-3-3σ orchestrates a functional interaction of TGFβ/Smad3 with p53, plays a role in the maintenance of cancer stem cells and could provide a new potential target for intervention in breast cancer.
|
23741479 |
2013 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Expression of the TGF-β signaling mediator SMAD3 varied inversely with Weiss score, so that SMAD3 expression was lowest in the most malignant tumors.
|
23866946 |
2013 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Smad3 is often underexpressed in very diverse types of malignant tumors and has an important tumor suppressive function; however, the underlying mechanism in solid cancer including glioblastomas(GBM) is not fully explored.
|
23892108 |
2013 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Real time PCR was used to measure mRNA expression of Smad2 and Smad3 in cancer and surrounding non-tumor tissue.
|
22539990 |
2012 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Functional interaction between Smad3 and S100A4 (metastatin-1) for TGF-beta-mediated cancer cell invasiveness.
|
20070253 |
2010 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Knockdown of Smad3 by siRNA decreases activin A-promoted AR expression and cancer cell migration.
|
19257827 |
2009 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Mechanisms of action of TGF-beta in cancer: evidence for Smad3 as a repressor of the hTERT gene.
|
17934056 |
2007 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Canonical TGF-beta is involved in cell differentiation, tissue maintenance, and wound healing, but also plays a central role in the pathogenesis of diseases such as cancer Here we describe a lentivirus-based reporter vector system expressing green fluorescent protein (GFP) or red fluorescent protein (RFP) under the control of a Smad3-responsive element (CAGA)12 that allows observation of the temporospatial pattern of endogeneous Smad3-mediated signaling on a cellular level.
|
17907571 |
2007 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
To our knowledge, this is the first report of Smad3 mutation in human malignancy.
|
16828225 |
2007 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Engineering the interface between Smad3 and hTERT gene may lead to a new strategy to inhibit telomerase activity in cancer.
|
16474430 |
2006 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Mutations of Smad4 that render it defective in heterodimerization with Smad3, which are found in many human cancers, convert the activity of Smad3 on the snoN promoter from inhibitory to stimulatory, resulting in increased snoN expression in cancer cells.
|
16314499 |
2005 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Our present data based on selective interference with activation of endogenous Smad2 and Smad3 by stable expression of a mutant form of the TGF-beta type I receptor (RImL45) unable to bind Smad2/3 but with a functional kinase again show that reduction in Smad2/3 signaling by expression of RImL45 enhanced the malignancy of xenografted tumors of the well-differentiated MCF10A-derived tumor cell line MCF10CA1h, resulting in formation of larger tumors with a higher proliferative index and more malignant histologic features.
|
15231662 |
2004 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
TGF-beta-induced nuclear localization of Smad2 and Smad3 in Smad4 null cancer cell lines.
|
12618756 |
2003 |