|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
TK1, TRIP13 and OCT4 were found to exhibit concurrent higher expression levels in HCC tumors than in APTs.
|
31848930 |
2020 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
Our findings demonstrate that tumor-suppressor proteins Oct4 and SOX2 have a prominent expression profile in the primary stage of cancer, but, in the metastatic stage, their expression is downregulated, leading to the failure to prevent metastatic cancer.
|
31646784 |
2020 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
In a human lung cancer xenograft model, Oct4-overexpressing tumors expressed elevated levels of Egr1.
|
31399076 |
2019 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
These results were reflected by decreased E‑cadherin expression and increased N‑cadherin expression, along with increased cell migration, promoted cell proliferation ability and elevated relative protein expression of Oct4 and Nanog, and accelerated tumor growth, accompanied by a higher number of metastatic nodes.
|
31485592 |
2019 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
After the treatment period, the tumor tissues were weighed and harvested for mRNA and protein isolation. qPCR and Western blotting were used to evaluate the expression of cancer stemness markers (epithelial cell adhesion molecule [EpCAM], cluster of differentiation [CD13], CD90, aldehyde dehydrogenase 1 [ALDH1], CD44, and CD45), totipotency factors (sex determining region Y-box 2 [Sox2], Nanog, and octamer-binding transcription factor 4 [Oct4]), and genes involved in the Notch, Wnt/<i>β</i>-catenin, Hedgehog, and Hippo signaling pathways.
|
31341493 |
2019 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
The ZnAs@SiO<sub>2</sub> NPs also inhibited tumor spheroid formation <i>in vitro</i> and tumor initiation <i>in vivo</i> and induced significant changes in the expression of stemness markers (CD133, Sox-2, and Oct-4) and EMT markers (E-cadherin, Vimentin, and Slug) both <i>in vitro</i> and <i>in vivo.</i> These effects of ZnAs@SiO<sub>2</sub> that correlated with prognosis of HCC were mediated by the SHP-1/JAK2/STAT3 signaling.
|
31285768 |
2019 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
Finally, we examined the correlation between HER2 status and stem cell-related genes expression in human ovarian tumor tissues, and found that expressions of OCT4, COX2, and Nanog were higher in HER2 positive tumors than in HER2 negative tumors.
|
30314995 |
2019 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
In vivo, tumor volume and tumor weight were decreased, while tumor necrosis and tumor apoptosis were increased in OCT4&SOX2 CTLs group than CMV pp65 CTLs group and control group, and in OCT4&SOX2 CTLs + PD-1 inhibitor group than OCT4&SOX2 CTLs group and PD-1 inhibitor group.
|
30382588 |
2019 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
Expression of master transcriptional regulators of stem cells (Oct4 and Sox2) is associated with mediating tumor proliferation and tumor differentiation.
|
31115051 |
2019 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
GLPG1790 down-modulated the expression of mesenchymal markers CD44, Sox2, nestin, octamer-binding transcription factor 3/4 (Oct3/4), Nanog, CD90, and CD105, and up-regulated that of glial fibrillary acidic protein (GFAP) and pro-neural/neuronal markers, βIII tubulin, and neurofilaments.GLPG1790 reduced tumour growth in vivo.
|
30871240 |
2019 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
Using genetic-lineage-tracing experiments and an in situ labeling approach, we show that DDR-induced epigenetic reactivation of OCT4 regulates the resistance to chemotherapy and contributes to tumor relapse both in mouse and primary human cancers.
|
30954402 |
2019 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
Knockdown of OCT4 also reduced stemness of GCTs, as assessed by the expression of other stemness factors, alkaline phosphatase staining, and tumour sphere formation ability.
|
30078675 |
2018 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
Meanwhile, FoxM1 linked closely with the expression levels of stem cell markers including Nanog, Sox2, and OCT4 in tumor samples, and also promoted the expression of these stemness-related genes <i>in vitro</i>.
|
30416986 |
2018 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
In addition, DOX induced cell senescence and reduced tumor sphere formation and the proportion of NANOG- and OCT4-positive cells after 7 days.
|
28612256 |
2018 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
GeneticVariation |
BEFREE |
Ubiquitination-defective mutant of OCT4(K284R) overexpressed cells drastically generated tumor burdens in mice.
|
29511337 |
2018 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
Octamer‑binding transcription factor 4 (Oct4) has been identified as a novel transcription factor associated with tumorigenesis, acquisition and maintenance of cancer stem cell characteristics and poor prognosis in tumors.
|
29901157 |
2018 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
In summary, Oct4 was related to tumor differentiation and later Dukes stage in colon cancer, and was correlated with invasion of lymphatic only in RCC.
|
29656661 |
2018 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
In specimens from patients with colorectal cancer, the expressions of cellular prion protein (PrP<sup>C</sup> ) and Oct4 were significantly correlated with metastasis and tumor stages.
|
30091203 |
2018 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
Functionally, the gain and loss-of-functional experiments revealed that LINC00511 promoted the proliferation, sphere-formation ability, stem factors (Oct4, Nanog, SOX2) expression and tumor growth in breast cancer cells.
|
30482236 |
2018 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
Accordingly, LKB1-null breast cancer cells exhibited an increased ability to form mammospheres and elevated expression of pluripotency-factors (Oct4, Nanog and Sox2), properties also observed in spontaneous tumors in Lkb1<sup>-/-</sup> mice.
|
28581518 |
2017 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
Altogether, our data highlights an unprecedented role for OCT4 as central regulator of mitotic fidelity and RB tumor suppressor pathway activity.
|
28319064 |
2017 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
We propose that Oct3/4, Sox2 and Nanog are associated with tumor hypoxia characterized in oral SCC and that these factors may also contribute to the undifferentiated potency observed in oral SCC clinically.
|
28314267 |
2017 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
Phagocytosis of apoptotic cancer cells by macrophages resulted in their transformation into tumor stem (initiating)-like cells, as indicated by the expression of epithelial markers (e.g., cytokeratin) and stem cell markers (e.g., Oct4) and their capability to differentiate <i>in vitro</i> and self-renew in serum-free media.
|
29137267 |
2017 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
Biomarker |
BEFREE |
Treatment of tumor-bearing mice with genotoxic chemotherapy not only prolonged survival and reduced tumor size but also selectively eliminated the OCT4-positive cancer stem cells.
|
29141221 |
2017 |
|
POU5F1P3
|
Neoplasms
|
0.100 |
AlteredExpression |
BEFREE |
AFMSCs exhibited positive OCT4 expression and were not observed to induce tumor development in nude mice.
|
28849231 |
2017 |