|
PITT-HOPKINS SYNDROME
|
1.000 |
GeneticVariation
|
disease |
BEFREE |
As mutations in TCF4 cause Pitt-Hopkins syndrome (PTHS) characterized by severe intellectual disability, our data also potentially provide insights into the basis of neurological defects linked to TCF4 mutations.
|
31845732 |
2019 |
|
Neoplasm Metastasis
|
0.070 |
Biomarker
|
phenotype |
BEFREE |
In summary, our study demonstrated that the positive feedback loop of ZEB1/HDGF/β-catenin/TCF4 plays an unfavorable role in the metastasis of endometrial carcinoma.
|
31815037 |
2019 |
|
Endometrial Carcinoma
|
0.060 |
Biomarker
|
disease |
BEFREE |
In summary, our study demonstrated that the positive feedback loop of ZEB1/HDGF/β-catenin/TCF4 plays an unfavorable role in the metastasis of endometrial carcinoma.
|
31815037 |
2019 |
|
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.030 |
Biomarker
|
disease |
BEFREE |
Mechanistically, calcitriol suppressed EMT through different signaling pathways: (1) calcitriol suppressed Smad2/3 phosphorylation through reinforcing physical interaction between vitamin D receptor (VDR) and Smad3 in TGF-β1-stimulated RCC cells; (2) calcitriol inhibited STAT3 activation in LPS-stimulated RCC cells; (3) calcitriol inhibited β-catenin/TCF-4 activation through promoting integration of VDR with β-catenin in TGF-β1-unstimulated RCC cells.
|
31729097 |
2020 |
|
Renal Cell Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Mechanistically, calcitriol suppressed EMT through different signaling pathways: (1) calcitriol suppressed Smad2/3 phosphorylation through reinforcing physical interaction between vitamin D receptor (VDR) and Smad3 in TGF-β1-stimulated RCC cells; (2) calcitriol inhibited STAT3 activation in LPS-stimulated RCC cells; (3) calcitriol inhibited β-catenin/TCF-4 activation through promoting integration of VDR with β-catenin in TGF-β1-unstimulated RCC cells.
|
31729097 |
2020 |
|
Degenerative polyarthritis
|
0.030 |
Biomarker
|
disease |
BEFREE |
Knockdown of MFI2-AS1 increased cell viability but suppressed apoptosis, inflammatory response and extracellular matrix degradation in LPS-treated chondrocytes by increasing miR-130a-3p and decreasing TCF4, indicating a novel target for the treatment of osteoarthritis.
|
31678554 |
2020 |
|
Liver carcinoma
|
0.200 |
AlteredExpression
|
disease |
BEFREE |
Correction to: KIFC1 is activated by TCF-4 and promotes hepatocellular carcinoma pathogenesis by regulating HMGA1 transcriptional activity.
|
31666105 |
2019 |
|
Malignant tumor of colon
|
0.100 |
Biomarker
|
disease |
BEFREE |
Together, these data suggest that γ-Mangostin inhibits colon cancer growth through targeting TCF4.
|
31608135 |
2019 |
|
Colon Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Together, these data suggest that γ-Mangostin inhibits colon cancer growth through targeting TCF4.
|
31608135 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Since bioinformatics analysis indicated TCF4 as a novel target of miR-139-5p, our mechanistic studies validated this, and confirmed that TCF4 restoration could attenuate the tumor inhibitory activities of miR-139-5p in CC progression, and recover the normal Wnt/β-catenin signaling.
|
31571923 |
2019 |
|
Malignant tumor of cervix
|
0.020 |
Biomarker
|
disease |
BEFREE |
Since bioinformatics analysis indicated TCF4 as a novel target of miR-139-5p, our mechanistic studies validated this, and confirmed that TCF4 restoration could attenuate the tumor inhibitory activities of miR-139-5p in CC progression, and recover the normal Wnt/β-catenin signaling.
|
31571923 |
2019 |
|
Cervix carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Since bioinformatics analysis indicated TCF4 as a novel target of miR-139-5p, our mechanistic studies validated this, and confirmed that TCF4 restoration could attenuate the tumor inhibitory activities of miR-139-5p in CC progression, and recover the normal Wnt/β-catenin signaling.
|
31571923 |
2019 |
|
cervical cancer
|
0.020 |
Biomarker
|
disease |
BEFREE |
Since bioinformatics analysis indicated TCF4 as a novel target of miR-139-5p, our mechanistic studies validated this, and confirmed that TCF4 restoration could attenuate the tumor inhibitory activities of miR-139-5p in CC progression, and recover the normal Wnt/β-catenin signaling.
|
31571923 |
2019 |
|
Fuchs Endothelial Dystrophy
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Seventy percent of FECD cases are due to an intronic CTG expansion within the TCF4 gene, resulting in accumulation of CUG repeat RNA nuclear foci in corneal endothelium.
|
31560764 |
2019 |
|
Corneal dystrophy, Fuchs' endothelial, 1
|
0.040 |
Biomarker
|
disease |
BEFREE |
Quantitative Studies of Muscleblind Proteins and Their Interaction With TCF4 RNA Foci Support Involvement in the Mechanism of Fuchs' Dystrophy.
|
31560764 |
2019 |
|
Fuchs Endothelial Dystrophy
|
0.500 |
Biomarker
|
disease |
BEFREE |
The association of TNR expansion in TCF4 with FECD is shown for the first time in the Thai population.
|
31554942 |
2019 |
|
Colorectal Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We then focused on transcription factor 4 (TCF4) as it is downregulated in CRC and associated with increased stemness in tumors.
|
31540772 |
2019 |
|
Prostate carcinoma
|
0.120 |
Biomarker
|
disease |
BEFREE |
Taken together, the current results indicate that TCF4 induces enzalutamide resistance via NED in CaP.
|
31536510 |
2019 |
|
Malignant neoplasm of prostate
|
0.020 |
Biomarker
|
disease |
BEFREE |
Taken together, the current results indicate that TCF4 induces enzalutamide resistance via NED in CaP.
|
31536510 |
2019 |
|
Schizophrenia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Deconvolution of transcriptional networks identifies TCF4 as a master regulator in schizophrenia.
|
31535015 |
2019 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.030 |
Biomarker
|
disease |
BEFREE |
Kruppel-Like Transcription Factor-4 Gene Expression and DNA Methylation Status in Type 2 Diabetes and Diabetic Nephropathy Patients.
|
31495395 |
2019 |
|
Colorectal Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We studied thirteen single nucleotide polymorphisms (SNPs) located in SFRP3 (rs7775), CTNNB1 (β-catenin) [rs4135385, rs13072632], APC (rs454886, rs459552), LRP6 (rs2075241, rs2284396), DKK4 (rs3763511), DKK3 (rs6485350), TCF4 (rs12255372) and AXIN2 (rs3923086, rs3923087, rs4791171) in patients with colorectal cancer (n = 122) and controls (n = 110).
|
31485167 |
2019 |
|
Malignant neoplasm of colon and/or rectum
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We studied thirteen single nucleotide polymorphisms (SNPs) located in SFRP3 (rs7775), CTNNB1 (β-catenin) [rs4135385, rs13072632], APC (rs454886, rs459552), LRP6 (rs2075241, rs2284396), DKK4 (rs3763511), DKK3 (rs6485350), TCF4 (rs12255372) and AXIN2 (rs3923086, rs3923087, rs4791171) in patients with colorectal cancer (n = 122) and controls (n = 110).
|
31485167 |
2019 |
|
Fuchs Endothelial Dystrophy
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Identification of novel splicing patterns and differential gene expression in RE+/FECD- samples provides new insights and more relevant gene targets that may be protective against FECD disease in vulnerable patients with TCF4 CTG TNR expansions.
|
31469403 |
2019 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Furthermore, restored TCF-4 expression rescued the inhibitory roles of miR-379 overexpression on cell proliferation, migration, and invasion.Our study for the first time demonstrated that miR-379/TCF-4 might involve in the progression of laryngeal carcinoma, and miR-379 appears to serve as a novel tumor suppressor in laryngeal carcinoma.
|
31436384 |
2019 |