|
Carcinogenesis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
This work reveals a novel role of Mettl14 and N<sup>6</sup>-methyladenosine in bladder tumorigenesis and bladder TICs, adding new layers for bladder TIC regulation and N<sup>6</sup>-methyladenosine function.
|
31760940 |
2019 |
|
Carcinogenesis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
This demonstrated that EBV hijacks METTL14 to drive EBV-mediated tumorigenesis.
|
31226160 |
2019 |
|
Carcinogenesis
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
Knockdown of METTL3 or METTL14, key components of the RNA methyltransferase complex, dramatically promotes human GSC growth, self-renewal, and tumorigenesis.
|
28297667 |
2017 |
|
Neoplasm Metastasis
|
0.020 |
AlteredExpression
|
phenotype |
BEFREE |
METTL14 knockdown significantly reduced m6A levels in total RNAs and promoted CRC cell growth and metastasis, whereas METTL14 overexpression markedly increased m6A levels in total RNA and inhibited CRC cell growth and metastasis.
|
31839484 |
2020 |
|
Tumor Cell Invasion
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
We also verified that METTL14 suppressed CRC cell growth via the miR-375/Yes-associated protein 1 (YAP1) pathway, as well as inhibited CRC cell migration and invasion through the miR-375/SP1 pathway.
|
31839484 |
2020 |
|
Malignant Neoplasms
|
0.020 |
Biomarker
|
group |
BEFREE |
The expression of m6A methylases (METTL3, METTL14 and WTAP) and demethylases (FTO and ALKBH5) were analyzed by using ONCOMINE and The Cancer Genome Atlas databases and in 36 pairs of BC and adjacent non-cancerous tissue.
|
30953473 |
2019 |
|
Neoplasms
|
0.020 |
Biomarker
|
group |
BEFREE |
Mettl14 knockout promotes the proliferation, self-renewal, metastasis and tumor initiating capacity of bladder TICs, and Mettl14 overexpression exerts an opposite role.
|
31760940 |
2019 |
|
Neoplasms
|
0.020 |
Biomarker
|
group |
BEFREE |
METTL14 was also significantly induced in EBV-positive tumors, promoted growth of EBV-transformed cells and tumors in Xenograft animal models.
|
31226160 |
2019 |
|
Primary malignant neoplasm
|
0.020 |
Biomarker
|
group |
BEFREE |
The expression of m6A methylases (METTL3, METTL14 and WTAP) and demethylases (FTO and ALKBH5) were analyzed by using ONCOMINE and The Cancer Genome Atlas databases and in 36 pairs of BC and adjacent non-cancerous tissue.
|
30953473 |
2019 |
|
Malignant Neoplasms
|
0.020 |
Biomarker
|
group |
BEFREE |
We report that altering m<sup>6</sup>A levels by silencing either <i>N</i><sup>6</sup>-adenosine methyltransferase METTL14 (methyltransferase-like 14) or demethylase ALKBH5 (ALKB homolog 5) inhibits cancer growth and invasion.
|
30306128 |
2018 |
|
Tumor Cell Invasion
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
We report that altering m<sup>6</sup>A levels by silencing either <i>N</i><sup>6</sup>-adenosine methyltransferase METTL14 (methyltransferase-like 14) or demethylase ALKBH5 (ALKB homolog 5) inhibits cancer growth and invasion.
|
30306128 |
2018 |
|
Primary malignant neoplasm
|
0.020 |
Biomarker
|
group |
BEFREE |
We report that altering m<sup>6</sup>A levels by silencing either <i>N</i><sup>6</sup>-adenosine methyltransferase METTL14 (methyltransferase-like 14) or demethylase ALKBH5 (ALKB homolog 5) inhibits cancer growth and invasion.
|
30306128 |
2018 |
|
Neoplasm Metastasis
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
These studies reveal an important role of METTL14 in tumor metastasis and provide a fresh view on m<sup>6</sup> A modification in tumor progression.(Hepatology 2017;65:529-543).
|
27774652 |
2017 |
|
Tumor Progression
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
Moreover, inhibition of FTO suppresses tumor progression and prolongs lifespan of GSC-grafted mice substantially. m<sup>6</sup>A sequencing reveals that knockdown of METTL3 or METTL14 induced changes in mRNA m<sup>6</sup>A enrichment and altered mRNA expression of genes (e.g., ADAM19) with critical biological functions in GSCs.
|
28297667 |
2017 |
|
Tumor Progression
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
These studies reveal an important role of METTL14 in tumor metastasis and provide a fresh view on m<sup>6</sup> A modification in tumor progression.(Hepatology 2017;65:529-543).
|
27774652 |
2017 |
|
Colorectal Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Taken together, our studies showed an important role for METTL14 in CRC progression and provided novel insight into m6A modification in CRC progression.
|
31839484 |
2020 |
|
Kidney Failure, Acute
|
0.010 |
Biomarker
|
disease |
BEFREE |
Mechanistically, we identified that YAP1 is a direct target of METTL14 in AKI progression.
|
31318098 |
2020 |
|
Acute lymphocytic leukemia
|
0.010 |
Biomarker
|
disease |
BEFREE |
The reduced levels of METTL3 and METTL14 suggest a possible role in the pathogenesis and course of E/R-positive ALL.
|
31429529 |
2019 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.010 |
Biomarker
|
disease |
BEFREE |
The reduced levels of METTL3 and METTL14 suggest a possible role in the pathogenesis and course of E/R-positive ALL.
|
31429529 |
2019 |
|
Malignant neoplasm of stomach
|
0.010 |
Biomarker
|
disease |
BEFREE |
Through in vitro experiments, we proved that m6A suppression (represented by METTL14 knockdown) promoted GC cell proliferation and invasiveness through activating Wnt and PI3K-Akt signaling, while m6A elevation (represented by FTO knockdown) reversed these phenotypical and molecular changes. m6A may also be involved in interferon signaling and immune responses of GC.
|
31243897 |
2019 |
|
Impaired glucose tolerance
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Acute deletion of Mettl14 in β-cells results in glucose intolerance as a result of a reduction in insulin secretion in β-cells even though β-cell mass is increased, which is related to increased β-cell proliferation.
|
31369074 |
2019 |
|
Vascular calcification
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
We used clinical human samples as well as rat models and primary human artery smooth muscle cell (HASMC) cultures to study the functional role of m6A and METTL14 in vascular calcification and in HASMCs.
|
31697949 |
2019 |
|
Stomach Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Through in vitro experiments, we proved that m6A suppression (represented by METTL14 knockdown) promoted GC cell proliferation and invasiveness through activating Wnt and PI3K-Akt signaling, while m6A elevation (represented by FTO knockdown) reversed these phenotypical and molecular changes. m6A may also be involved in interferon signaling and immune responses of GC.
|
31243897 |
2019 |
|
Adult Acute Lymphocytic Leukemia
|
0.010 |
Biomarker
|
disease |
BEFREE |
The reduced levels of METTL3 and METTL14 suggest a possible role in the pathogenesis and course of E/R-positive ALL.
|
31429529 |
2019 |
|
Precursor Cell Lymphoblastic Leukemia Lymphoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
The study of METTL3 and METTL14 expressions in childhood ETV6/RUNX1-positive acute lymphoblastic leukemia.
|
31429529 |
2019 |