|
Malignant neoplasm of breast
|
0.100 |
Biomarker
|
disease |
BEFREE |
EpCAM overexpression increases the expression of stemness markers (NANOG，SOX2, and OCT4) and EMT markers (N-cadherin and vimentin) under the condition of hypoxia in BC.
|
31584203 |
2020 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Since cancer stem cells (CSCs) are radioresistant and metastasis-initiating cells, we examined TGLI1 for its involvement in breast CSCs and found TGLI1 to transcriptionally activate stemness genes CD44, Nanog, Sox2, and OCT4 leading to CSC renewal, and TGLI1 outcompetes with GLI1 for binding to target promoters.
|
31462709 |
2020 |
|
Neoplasm Metastasis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Finally, Ku80 inhibits self-renewal and metastasis of hepatocellular carcinoma cells through breaking the SALL4-OCT4 interactions and down-regulating the expression of OCT4.
|
31816404 |
2020 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
TK1, TRIP13 and OCT4 were found to exhibit concurrent higher expression levels in HCC tumors than in APTs.
|
31848930 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
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 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
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 |
|
Breast Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
EpCAM overexpression increases the expression of stemness markers (NANOG，SOX2, and OCT4) and EMT markers (N-cadherin and vimentin) under the condition of hypoxia in BC.
|
31584203 |
2020 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Since cancer stem cells (CSCs) are radioresistant and metastasis-initiating cells, we examined TGLI1 for its involvement in breast CSCs and found TGLI1 to transcriptionally activate stemness genes CD44, Nanog, Sox2, and OCT4 leading to CSC renewal, and TGLI1 outcompetes with GLI1 for binding to target promoters.
|
31462709 |
2020 |
|
Liver carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
TK1, TRIP13 and OCT4 were found to exhibit concurrent higher expression levels in HCC tumors than in APTs.
|
31848930 |
2020 |
|
Malignant neoplasm of breast
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Analysis by qPCR, ELISA, western blot, immunofluorescence staining, sphere formation, colony assay, transwell migration, and invasion assays demonstrated rBmK AGAP treatment decreased the expressions of Oct4, Sox2, N-cadherin, Snail, and increased the expression of E-cadherin. rBmK AGAP inhibited breast cancer cell stemness, EMT, migration, and invasion by down-regulating PTX3 through NF-κB and Wnt/β-catenin signaling Pathway <i>in vitro</i> and <i>in vivo</i>.
|
30740360 |
2019 |
|
Malignant neoplasm of breast
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
PD-L1 could promote the expression of stemness markers (OCT4 and Nanog) in breast cancer stem cells.
|
30803931 |
2019 |
|
Malignant neoplasm of breast
|
0.100 |
Biomarker
|
disease |
BEFREE |
Correction to: Post-translational modification of OCT4 in breast cancer tumorigenesis.
|
31641242 |
2019 |
|
Malignant neoplasm of breast
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Downregulation of FOXD2‑AS1 decreased the percentage of CD44 antigen+/signal transducer CD24- in breast cancer stem cell (BCSC) cells, and decreased the expression of numerous stem factors, including Nanog, octamer‑binding transcription factor 4 (Oct4), and sex determining region Y‑box 2 (SOX2), and inhibited the epithelial‑mesenchymal transition process.
|
30628646 |
2019 |
|
Malignant neoplasm of breast
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
OCT4 was down-regulated in breast cancer tissues, and the overexpression of OCT4 promoted MDA-MB-231 cell proliferation and inhibited the proliferation of MCF-7 cells in vitro and in vivo, respectively.
|
31012189 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Hypoxia also enhanced the expression of cancer stem cell (CSC) transcription factors (NANOG, Oct4, SOX2), CD133 and EMT markers (N-cadherin, Vimentin), thereby supporting invasion.
|
31634481 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
D7-6 G cells had increased expression of cancer stem cells markers Oct4, Sox2, and Nanog; aldehyde dehydrogenase expression and activity; proportion of CD44<sup>+</sup>CD24<sup>-</sup>cells.
|
30579251 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The results demonstrated Wnt/β-catenin signaling was activated and was able to form mammospheres with increased cancer stem cell markers (ALDH1, NANOG, and OCT4) in endocrine-resistant cells.
|
31693936 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
POU5F1 (OCT4) is implicated in cancer stem cell self-renewal.
|
31012189 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Moreover, the nuclear localization of OCT3/4 protein in primordial follicle-enclosed oocytes suggests a possible increased activity of ovarian stem cells in response to chemotherapy and/or extragonadal cancer.
|
30857552 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Humanized Stem Cell Models of Pediatric Medulloblastoma Reveal an Oct4/mTOR Axis that Promotes Malignancy.
|
31786016 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We observed that miR-147 was downregulated in several colon cancer cell lines, and overexpressed miR-147 decreased the expression of cancer stem cell (CSC) markers OCT4, SOX2, and NANOG in the colon cancer cell lines HCT116 and SW480.
|
29426374 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In conclusion, our study suggested that bFGF/FGFR signalling plays an important role in maintaining lung cancer stem cell characteristics and regulating expression of cancer stem cell marker of OCT-4.
|
31282010 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
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 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Egr1 exerts a promoting effect on cancer metastasis in Oct4-overexpressing lung cancer.
|
31399076 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
CLIC4 expression is lowest in MKN45 cells，which have the highest tumorigenic potential and express the highest levels of cancer stem cell markers CD44 and OCT4, compared to N87 and AGS cells.
|
31560739 |
2019 |