|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
However, mechanisms as mutations in TGF-beta receptor II or Smad2 and 4 genes, frequently observed in other human cancers, have only rarely been observed in hepatocellular carcinomas.
|
11170302 |
2001 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The majority of Smad4 gene mutations in human cancer are missense, nonsense, and frameshift mutations at the mad homology 2 region (MH2), which interfere with the homo-oligomer formation of Smad4 protein and the hetero-oligomer formation between Smad4 and Smad2 proteins, resulting in disruption of TGFbeta signaling.
|
12821112 |
2003 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Furthermore, the analysis of the Cancer Genome Atlas data revealed that in CRC without microsatellite instability, overexpression of Myc and inactivation of Smads (including acquired mutations in SMAD2) are mutually exclusive, with odds ratio less than 0.1.
|
24627270 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<b>Background/Aims:</b> MiR-145 and Smad2 have been widely reported in the development and progression of human malignancies.
|
31114250 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our results demonstrated that TAMs contributed the EMT progression through a TGF-β/Smad2,3-4/Snail signaling pathway, and disrupting this pathway with TGF-β receptor inhibitor could suppress metastasis, readjusting our focus to the connection of TAMs and cancer metastasis.
|
29690747 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
At the molecular level, RBBP9 activity overcomes TGF-beta-mediated antiproliferative signaling by reducing Smad2/3 phosphorylation, a previously unknown role for a serine hydrolase in cancer biology.
|
20080647 |
2010 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Similar to TGFβ1, chemotherapeutics were found to stimulate Smad2/3 phosphorylation, cell migration, and markers related to epithelial-mesenchymal transition (EMT) and cancer stem cells (CSC).
|
29549162 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We show that interference with endogenous Smad2/3 signaling enhances the malignancy of xenografted tumors of premalignant and well-differentiated tumor cells but strongly suppresses lung metastases of more aggressive carcinoma cells after tail vein injection.
|
14678987 |
2003 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In the present study, we first intended to resolve the role of the hsMAD2 gene in human cancer by determining the potential presence of hsMAD2 mutations in 44 primary bladder tumors, 42 soft-tissue sarcomas and 10 hepatocellular carcinomas.
|
11400114 |
2001 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In previous reports, we described that DPC4/Smad4 and Smad2 are mutated in a fraction of human lung cancers and suggested possible roles of the downstream mediators of transforming growth factor-beta (TGF-beta)-elicited signals in the pathogenesis of this most common cancer.
|
9466656 |
1998 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We previously reported that aberrant TGF-β/Smad2/3 signaling in endometrial cancer (ECA) leads to continuous ubiquitylation of p27(kip1)(p27) by the E3 ligase SCF-Skp2/Cks1 causing its degradation, as a putative mechanism involved in the pathogenesis of this cancer.
|
26963853 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
1) CHI3L1 promoted cancer cell proliferation by regulating cell cycles; 2) CHI3L1 promoted cancer cell invasion and metastasis; 3) CHI3L1 regulate liver cancer potentially by regulating the TGF-β signaling pathways; 4) CHI3L1 has direct kinase activities or activate kinase to phosphorylate SMAD2, SMAD3.
|
30301907 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Aberrant function of Smad2, a crucial member of transforming growth factor beta (TGF-β) signaling, is associated with the development of malignancies, particularly in the gastrointestinal district.
|
31387321 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
CNVs of Smad2 showed statistical differences between cancer samples (both SCC and BCC) and normal tissues (p<0.05).
|
22301403 |
2012 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
SMAD family member 2 (SMAD2) is a key element downstream of the transforming growth factor beta (TGF-β) signaling pathway that regulates cancer metastasis by promoting the epithelial-mesenchyme transition (EMT).
|
31762811 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here we investigated the role of DLX2 in association with radiation-induced epithelial to mesenchymal transition (EMT) and stem cell-like properties and its regulation by Smad2/3 signaling in irradiated A549 and MDA-MB-231 human cancer cell lines.
|
26799321 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
TGF-beta-induced nuclear localization of Smad2 and Smad3 in Smad4 null cancer cell lines.
|
12618756 |
2003 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Smad5 homologs Smad2 and DPC4 have recently been linked to human cancer.
|
9264367 |
1997 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Smad2 is a key element downstream of the TGF-β signaling pathway to regulate cancer metastasis by promoting epithelial to mesenchymal transition and maintaining the cancer stem cell (CSC) phenotype.
|
25980495 |
2015 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
At least two different Smads, Smad2 and Smad4 (DPC4), have been implicated in human cancer and appear to have tumour-suppressor functions.
|
9862572 |
1998 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The top three ranked differential pathways were CREB phosphorylation, attachment of GPI anchor to urokinase plasminogen activator receptor (uPAR) and loss of function of SMAD2/3 in cancer.
|
28039715 |
2017 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This process includes the induction of Smad2/3 phosphorylation, the increase of Smad2/3 transcriptional activity and the upregulation of the expression of target genes involved in EMT and cancer progression (such as TGF-β1, MMP-2, MMP-9, plasminogen activator inhibitor type-1, vascular endothelial growth factor, Snail and Slug), thus promoting cancer cell mobility and invasion.
|
21441952 |
2011 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
External validation by mRNA expression showed a good agreement between hypermethylation in cancer and down-regulated mRNA expression of the genes EDNRB1, GPC6 and SMAD2, and between hypomethylation and up-regulated mRNA expression of the CASP8 and DCLRE1C genes.
|
24811787 |
2014 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
SGPP1 and Smad2 at mRNA and protein levels were negatively correlated with miR-27a in human colorectal cancer tissues and cancer cell lines.
|
25166914 |
2014 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Cell survival, cell cycle, numbers of side population (SP) cells and expression of the cancer stem cell marker cluster of differentiation (CD)133, epithelial-mesenchymal transition markers (E-cadherin, α-smooth muscle actin and vimentin) and TGF-β-regulated proteins [phospho-c-Jun N-terminal kinase (p-JNK), p-c-Jun and p-smad2] were investigated.
|
29805610 |
2018 |