|
Fibroid Tumor
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
The miR-29c and its target gene TGF-β3 in leiomyoma and the effects of TGF-β3 and blockade of DNMT1 on miR-29c expression.
|
31843095 |
2019 |
|
Uterine Fibroids
|
0.030 |
AlteredExpression
|
group |
BEFREE |
The miR-29c and its target gene TGF-β3 in leiomyoma and the effects of TGF-β3 and blockade of DNMT1 on miR-29c expression.
|
31843095 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Previously we demonstrated that polyphyllin I (PPI), a bioactive component extracted from Paris polyphylla, inhibited the growth of non-small cell lung cancer (NSCLC) cells through the SAPK/JNK-mediated suppressing p65, DNMT1 and EZH2 expressions.
|
31819506 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
DNMT1 recruited by EZH2-mediated silencing of miR-484 contributes to the malignancy of cervical cancer cells through MMP14 and HNF1A.
|
31810492 |
2019 |
|
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our finding characterizes miR-484 as a key suppressive regulator in CC metastasis and reveals a DNMT1-mediated epigenetic mechanism for miR-484 silencing, expanding our understanding of the molecular mechanism underlying CC progression and metastasis.
|
31810492 |
2019 |
|
Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Thus, miR-484, who is downregulated by DNMT1-mediated hypermethylation in its promoter, functions as a tumor suppressor by inhibiting MMP14 and HNF1A expression in CC.
|
31810492 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
DNMT1 recruited by EZH2-mediated silencing of miR-484 contributes to the malignancy of cervical cancer cells through MMP14 and HNF1A.
|
31810492 |
2019 |
|
Cervix carcinoma
|
0.080 |
Biomarker
|
disease |
BEFREE |
Our finding characterizes miR-484 as a key suppressive regulator in CC metastasis and reveals a DNMT1-mediated epigenetic mechanism for miR-484 silencing, expanding our understanding of the molecular mechanism underlying CC progression and metastasis.
|
31810492 |
2019 |
|
cervical cancer
|
0.070 |
Biomarker
|
disease |
BEFREE |
Our finding characterizes miR-484 as a key suppressive regulator in CC metastasis and reveals a DNMT1-mediated epigenetic mechanism for miR-484 silencing, expanding our understanding of the molecular mechanism underlying CC progression and metastasis.
|
31810492 |
2019 |
|
Malignant tumor of cervix
|
0.060 |
Biomarker
|
disease |
BEFREE |
Our finding characterizes miR-484 as a key suppressive regulator in CC metastasis and reveals a DNMT1-mediated epigenetic mechanism for miR-484 silencing, expanding our understanding of the molecular mechanism underlying CC progression and metastasis.
|
31810492 |
2019 |
|
Malignant tumor of colon
|
0.400 |
Biomarker
|
disease |
BEFREE |
5-Aza-CdR Regulates RASSF1A By Inhibiting DNMT1 To Affect Colon Cancer Cell Proliferation, Migration And Apoptosis.
|
31807076 |
2019 |
|
Colon Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
5-Aza-CdR Regulates RASSF1A By Inhibiting DNMT1 To Affect Colon Cancer Cell Proliferation, Migration And Apoptosis.
|
31807076 |
2019 |
|
Neurodegenerative Disorders
|
0.050 |
GeneticVariation
|
group |
BEFREE |
Recently, several mutations in the RFTS domain were shown to be causal for two adult onset neurodegenerative diseases; however, little is known about the impact of these mutations on the structure and function of DNMT1.
|
31804802 |
2019 |
|
Hypertensive disease
|
0.030 |
Biomarker
|
group |
BEFREE |
The AIM HY-INFORM study is part of the Informative Markers in Hypertension (AIM HY) Programme and comprises two crossover trials, each with a planned recruitment of 600 participants.
|
31791376 |
2019 |
|
Carcinogenesis
|
0.300 |
Biomarker
|
phenotype |
BEFREE |
The DNA methyltransferase 1 (DNMT1)/miR-34a axis promoted carcinogenesis of various types of cancers.
|
31781245 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the current study we determined the effects of treating KG-1 and U937 acute myeloid leukemia (AML) cells, in vitro, with the HDAC inhibitor, suberoylanilide hydroxamic acid (SAHA), or with a DNMT inhibitor, decitabine (DAC), or their combination, on cell proliferation, cell cycle progression, apoptosis, and expression of apoptosis-related proteins.
|
31766421 |
2019 |
|
Autistic Disorder
|
0.020 |
Biomarker
|
disease |
BEFREE |
Project AIM: Autism intervention meta-analysis for studies of young children.
|
31763860 |
2020 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The results showed that curcumin combined with 5 μM DAC may inhibit cancer cell colony formation, migration through EMT (epithelial-mesenchymal transition) process regulation, total DNMT activity, especially in DNMT3a protein expression, and may also regulate tumor suppressor gene SFRP5 expression involved in the Wnt/β-catenin signaling pathway.
|
31754130 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The results showed that curcumin combined with 5 μM DAC may inhibit cancer cell colony formation, migration through EMT (epithelial-mesenchymal transition) process regulation, total DNMT activity, especially in DNMT3a protein expression, and may also regulate tumor suppressor gene SFRP5 expression involved in the Wnt/β-catenin signaling pathway.
|
31754130 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The results showed that curcumin combined with 5 μM DAC may inhibit cancer cell colony formation, migration through EMT (epithelial-mesenchymal transition) process regulation, total DNMT activity, especially in DNMT3a protein expression, and may also regulate tumor suppressor gene SFRP5 expression involved in the Wnt/β-catenin signaling pathway.
|
31754130 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our study showed a molecular mechanism of DNMT1 in linking tumor metabolic reprogramming to the Hippo-TAZ pathway and functional significance of the DNMT1-TAZ feedback loop in the migratory and invasive potential of lung cancer cells.
|
31746077 |
2020 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A reason to pursue this molecular-targeted effect instead of the DNA damage/cytotoxicity produced with high concentrations/doses, is that non-cytotoxic DNMT1-depletion can cytoreduce even p53-null myeloid malignancies while sparing normal haematopoiesis.
|
31736067 |
2020 |
|
Myeloid neoplasm
|
0.010 |
Biomarker
|
disease |
BEFREE |
We thus identified minimum doses of decitabine (0·1-0·2 mg/kg) that deplete DNMT1 without off-target anti-metabolite effects/cytotoxicity, and then administered these well-tolerated doses frequently 1-2X/week to increase S-phase dependent DNMT1-depletion, and used a Myeloid Malignancy Registry to evaluate long-term outcomes in 69 patients treated this way.
|
31736067 |
2020 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The association between DNA methyltransferases (DNMTs) genes polymorphisms and diseases in which DNA methylation plays a role in their pathogenesis has been described (e.g., cancer); however, its relationship with OA has not been investigated.
|
31713648 |
2020 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The association between DNA methyltransferases (DNMTs) genes polymorphisms and diseases in which DNA methylation plays a role in their pathogenesis has been described (e.g., cancer); however, its relationship with OA has not been investigated.
|
31713648 |
2020 |