|
POU5F1P3
|
Carcinogenesis
|
0.100 |
Biomarker |
BEFREE |
Though Oct4 and Nanog are homebox transcription factors essential to the self-renewal of stem cells and are expressed in several cancers, the role of Oct4/Nanog signaling in tumorigenesis is still elusive.
|
21159654 |
2010 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
AlteredExpression |
BEFREE |
Reactivation of OCT4 expression is postulated to occur in differentiated cells that have undergone tumorigenesis.
|
21480394 |
2012 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
Biomarker |
BEFREE |
Reprogramming with octamer-binding protein 4 and Jun dimerization protein 2 can inhibit tumorigenesis by switching off BMP7.Stem Cells 2017;35:2115-2128.
|
28782268 |
2017 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
AlteredExpression |
BEFREE |
Our results suggest that pseudogenes Oct4-pg5 and Oct4-pg1 may be involved in the regulation of Oct4 gene activity thus might be pertinent to carcinogenesis.
|
16229821 |
2005 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
AlteredExpression |
BEFREE |
The strong expression of Oct4 and Nanog in metaplastic ducts and Oct4 expression preceding Ras mutation suggests that these homeobox transcription factors are associated with the early stage of pancreatic cancer carcinogenesis and may play an important role in that process.
|
20173672 |
2010 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
Biomarker |
BEFREE |
Octamer 4 (Oct4), a member of the Pit-Oct-Unc transcription factor family required to maintain self-renewal and pluripotency of embryonic stem cells, has been previously identified to be associated with tumorigenesis and malignant transformation of numerous types of cancer including hepatocellular carcinoma (HCC).
|
28454439 |
2017 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
Biomarker |
BEFREE |
Moreover, the cells demonstrate aberrant accumulation of wild type tumor-suppressor protein p53, indicating its functional inactivation, highly up-regulated levels of onco-protein cMYC and the BTIC marker OCT3/4, along with metabolic switch to glycolysis - suggesting that these changes occurred in the early stages of tumorigenesis.
|
29568390 |
2018 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
Biomarker |
BEFREE |
A similar treatment also modulated numerous microRNAs (miRs) including one regulator of Oct4 as well as miRs involved in oncogenesis and/or malignancy, with only a few estrogen-induced miRs.
|
27959387 |
2017 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
AlteredExpression |
BEFREE |
With the availability of normal adult human stem cells, tests for the expression of Oct3/4 gene and the stem cell theory in human carcinogenesis became possible.
|
17261754 |
2006 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
GeneticVariation |
BEFREE |
Furthermore, the data revealed an alteration in the subcellular distribution of Oct4, possibly due to the inhibition of cytoplasm-to-nucleus translocation during carcinogenesis.
|
22922943 |
2012 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
AlteredExpression |
BEFREE |
Our study demonstrated, for the first time, the expression of OCT-4 in bladder cancer and a further clue to the involvement of embryonic genes in carcinogenesis.
|
17205510 |
2007 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
Biomarker |
BEFREE |
Through an integrative approach combining our Oct4 chromatin-immunoprecipitation sequencing and ENCODE datasets, we identified the genome-wide binding regions of Oct4 in lung cancer at promoter and enhancer of numerous genes involved in critical pathways which promote tumorigenesis.
|
25609695 |
2015 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
Biomarker |
BEFREE |
OCT4, a homeobox transcription factor, is essential for self-renewal of embryonic stem cells, but little is known about the role of OCT4 in non-germ-cell tumorigenesis.
|
30209362 |
2019 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
AlteredExpression |
BEFREE |
MiR-9 promotes tumorigenesis and angiogenesis and is activated by MYC and OCT4 in human glioma.
|
30795814 |
2019 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
Biomarker |
BEFREE |
To investigate whether Oct4 and Nanog play crucial role in maintaining the stemness of PCSCs, double knockdown of Oct4 and Nanog demonstrated that Oct4 and Nanog significantly reduced proliferation, migration, invasion, chemoresistance, and tumorigenesis of PCSCs in vitro and in vivo.
|
23872274 |
2013 |
|
POU5F1P3
|
Carcinogenesis
|
0.100 |
AlteredExpression |
BEFREE |
Silencing FOXM1 inhibited the expression of Nanog, Oct4, and Sox2 in LCSCs by decreasing the expression of ALDH2. in vivo experiment, silencing FOXM1 suppressed tumorigenesis of LCSCs by decreasing the expression of ALDH2.
|
31580537 |
2020 |