|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We further demonstrated that inactivation of p38 is a potential mechanism contributing to acquisition and maintenance of cancer stem cell properties in non-small cell lung cancer (NSCLC) cells. p38, in particular the p38γ and p38δ isoforms, suppresses the cancer stem cell properties and tumor initiating ability of NSCLC cells by promoting the ubiquitylation and degradation of stemness proteins such as SOX2, Oct4, Nanog, Klf4 and c-Myc, through MK2-mediated phosphorylation of Hsp27 that is an essential component of the proteasomal degradation machinery.
|
28460458 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Krüppel-like factor 4 (KLF4) has been reported as a bi-regulator in malignancies, but little is known about its role in MCL.
|
28278702 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we initially showed that HBV stimulates the production of cancer stem cells (CSCs)-related markers (CD133, CD117 and CD90) and CSCs-related genes (Klf4, Sox2, Nanog, c-Myc and Oct4) and facilitates the self-renewal of CSCs in human hepatoma cells.
|
28455240 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Klf4 is dysregulated and displays divergent functions in multiple malignancies, but the biological roles of Klf4 in nasopharyngeal carcinoma (NPC) remain unknown.
|
29212199 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our findings support the idea that RYBP may represent a target for cancer therapy and suggest that it may be useful as a prognostic biomarker for HCC, either alone or in combination with KLF4 and Sp1.
|
28028181 |
2017 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The biological functions of MSI2 regarding PDAC cell growth, migration, invasion, and metastasis were studied using gain- and loss-of-function assays both in vitro and in vivo Regulation of MSI2 expression by KLF4 was examined in several cancer cell lines, and the underlying mechanisms were studied using molecular biologic methods.
|
27449499 |
2017 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Forced expression of KLF4 profoundly attenuated lung cell proliferation and cancer formation in a murine model.
|
27153563 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Further, various studies identified genes in cancer stem cells, which were previously shown to regulate the pluripotency circuitry, particularly the so-called "Yamanaka-Factors" (OCT4, KLF4, SOX2, and c-MYC).
|
26896855 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
For PrTIC enrichment, we induced cancer stem cell (CSC) properties in PrCa cells by transducing three defined factors (OCT3/4, SOX2, and KLF4), followed by culture with conventional serum-containing medium.
|
27113741 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
To identify novel factors that contribute to lung cancer pathogenesis, we analyzed a lung cancer database from The Cancer Genome Atlas and found that Krüppel-like Factor 4 (KLF4) expression is significantly lower in patients' lung cancer tissue than in normal lung tissue.
|
26113043 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, the use of KLF4 as a diagnostic and therapeutic target in cancer requires careful consideration of context.
|
26934576 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Among astrocytomas, mRNA expression of OCT4, MYC and (less robust) KLF4 increased with malignancy, while in recurrent glioblastomas MYC expression slightly decreased.
|
27600094 |
2016 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Significantly, we found that the expression of pluripotency factors Sox2, Oct4 and Klf4, as well as expression of cancer stem cell (CSC) marker CD133, in the Nanog-targeted HepG2 cells was markedly downregulated.
|
26676719 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
KLF4 and CD44 regulate cancer cell stemness, but their precise functions and roles in metastatic progression are not well understood.
|
26880805 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Therefore, for better therapeutics of cancer disease, it is crucial to develop a deeper understanding of the mechanisms of how KLF4 regulate CSC functions.
|
25987013 |
2015 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Along with these roles in normal cells and tissues, KLF4 has important tumor suppressive and oncogenic functions in some malignancies.
|
26517087 |
2015 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Although studies have shown that Oct4, Sox2, Klf4, and c-Myc (OKSM)-mediated induced pluripotent stem cell (iPSC) technology sensitizes cancer cells to drugs, the potential risk of inserting c-Myc and random insertions of exogenous sequences into the genome persists.
|
24740829 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The transcription factor Krüppel-like factor 4 (KLF4) has been implicated in human cancers as a tumor suppressor or oncogene, although its role depends greatly on the cellular context.
|
25137052 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
KLF4 may function as a tumor suppressor gene in urothelial cancer since down-regulation of KLF4 by promoter hypermethylation would promote cancer progression.
|
24018236 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The generation of induced pluripotent stem cells (iPSCs) from somatic cells by expressing ectopic reprogramming transcriptional factors such as Oct3/4, Sox2, Klf4, c-Myc, and Nanog is one of the cutting-edge discoveries in stem cell and cancer research.
|
24568610 |
2014 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Together these results identify a new mechanism of VEGF up-regulation in cancer that involves concomitant loss of KLF-4-HDAC-mediated transcriptional repression and active recruitment of SAF-1-mediated transcriptional activation.
|
23926105 |
2013 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Krüppel-like factor 4 (KLF4) is a transcription factor that can have divergent functions in different malignancies.
|
23722653 |
2013 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our laboratory also introduced four transcription factors (Oct3/4, Sox2, c-Myc and Klf4) into cancer cells, generating induced pluripotent cancer cells that exhibited strikingly less malignant features, suggesting the possibility of a novel type of cancer therapy.
|
22826352 |
2012 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The modulation of KLF4 expression may represent a novel therapeutic approach for β-catenin-driven malignancies.
|
22407433 |
2012 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Apart from their role in regular metabolism, abnormal profiles of miRNA expression accompany cancer transformation, including colorectal cancer (CRC) metastasis. microRNAs may play a role in each phase of CRC metastasis including angiogenesis, invasion, intravasation, circulation, extravasation and metastatic colonization. microRNA levels may serve as a predictive CRC marker, which was confirmed by the serum level of miR-29a targeting KLF4, a marker of cell stemness, and the plasma level of miR-221 down-regulating c-Kit, Stat5A and ETS1, which are signal transducers and transcription factor, respectively.
|
23173124 |
2012 |