Last update 21 Mar 2024
NANOG
Nanog homeobox
Last update 21 Mar 2024
Basic Info
Synonyms FLJ12581, FLJ40451, hNanog + [4] |
Introduction Transcription regulator involved in inner cell mass and embryonic stem (ES) cells proliferation and self-renewal. Imposes pluripotency on ES cells and prevents their differentiation towards extraembryonic endoderm and trophectoderm lineages. Blocks bone morphogenetic protein-induced mesoderm differentiation of ES cells by physically interacting with SMAD1 and interfering with the recruitment of coactivators to the active SMAD transcriptional complexes. Acts as a transcriptional activator or repressor. Binds optimally to the DNA consensus sequence 5'-TAAT[GT][GT]-3' or 5'-[CG][GA][CG]C[GC]ATTAN[GC]-3'. Binds to the POU5F1/OCT4 promoter (PubMed:25825768). Able to autorepress its expression in differentiating (ES) cells: binds to its own promoter following interaction with ZNF281/ZFP281, leading to recruitment of the NuRD complex and subsequent repression of expression. When overexpressed, promotes cells to enter into S phase and proliferation. |
Related
Target |
Mechanism |
Active Org. |
Originator Org. |
Active Indication |
Inactive Indication |
Drug Highest Phase |
First Approval Ctry. / Loc. |
First Approval Date |
A Phase II Clinical Study of BBI503 in Adult Patients With Advanced Gastrointestinal Stromal Tumors
A Phase II Clinical Study of BBI503 in Adult Patients With Advanced Urologic Malignancies
A Phase Ib/II Clinical Study of BBI503 in Combination With Selected Anti-Cancer Therapeutics in Adult Patients With Advanced Cancer
100 Clinical Results associated with NANOG
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100 Translational Medicine associated with NANOG
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01 Dec 2024Annals of medicine
MUC1-EGFR crosstalk with IL-6 by activating NF-κB and MAPK pathways to regulate the stemness and paclitaxel-resistance of lung adenocarcinoma.
Article
Author: Hongyu Xu ; Zedong Du ; Zhihui Li ; Xianguo Liu ; Xueting Li ; Xuan Zhang ; Jiayu Ma
BACKGROUND:
The chemotherapy resistance often leads to chemotherapy failure. This study aims to explore the molecular mechanism by which MUC1 regulates paclitaxel resistance in lung adenocarcinoma (LUAD), providing scientific basis for future target selection.
METHODS:
The bioinformatics method was used to analyse the mRNA and protein expression characteristics of MUC1 in LUAD. RT-qPCR and ELISA were used to detect the mRNA and protein expression, flow cytometry was used to detect CD133+ cells, and cell viability was detected by CCK-8 assay. The mRNA-seq was performed to analyse the changes in expression profile, GO and KEGG analysis were used to explore the potential biological functions.
RESULTS:
MUC1 is highly expressed in LUAD patients and is associated with a higher tumour infiltration. In paclitaxel resistance LUAD cells (A549/TAX cells), the expression of MUC1, EGFR/p-EGFR and IL-6 were higher than that of A549 cells, the proportion of CD133+ cells was significantly increased, and the expression of cancer stem cell (CSCs) transcription factors (NANOG, OCT4 and SOX2) were significantly up-regulated. After knocking down MUC1 in A549/Tax cells, the activity of A549/Tax cells was significantly decreased. Correspondingly, the expression of EGFR, IL-6, OCT4, NANOG, and SOX2 were significantly down-regulated. The mRNA-seq showed that knocking down MUC1 affected the gene expression, DEGs mainly enriched in NF-κB and MAPK signalling pathway.
CONCLUSION:
MUC1 was highly expressed in A549/TAX cells, and MUC1-EGFR crosstalk with IL-6 may be due to the activation of NF-κB and MAPK pathways, which promote the enrichment of CSCs and lead to paclitaxel resistance.
01 Mar 2024Oncology letters
OTUD7B knockdown inhibits the proliferation and stemness of breast cancer cells by destabilizing FOXM1.
Article
Author: Hebing Wang ; Sumei Han ; Jian Xiao ; Xinghang Fu ; Wenfeng Chen ; Dexiang Zhuo
Breast cancer is a leading cause of cancer-related death in women worldwide; therefore, there is an urgent need to develop novel therapies and drugs that prolong the survival and improve the quality of life of patients with breast cancer. In the present study, the effects and underlying mechanisms of OTU domain-containing 7B (OTUD7B) knockdown on breast cancer were investigated using MDA-MB-468, MDA-MB-453 and MCF7 cell lines. The results of Cell Counting Kit 8, colony formation and tumor sphere formation experiments showed that OTUD7B knockdown caused a significant decrease in the proliferation and sphere formation ability of MDA-MB-468, MDA-MB-453 and MCF7 cells in vitro. Moreover, western blotting results showed that CD44, EpCAM, SOX2 and Nanog protein levels were significantly decreased following OTUD7B knockdown. These findings indicated that OTUD7B knockdown reduced the proliferation and stemness of breast cancer cells. Co-immunoprecipitation assays demonstrated that OTUD7B interacted with forkhead box protein M1 (FOXM1) and reduced the polyubiquitylation of FOXM1 in breast cancer cells; accordingly, FOXM1 protein levels were significantly decreased by OTUD7B knockdown. Furthermore, the overexpression of FOXM1 reduced the inhibitory effects of OTUD7B knockdown on breast cancer cells. The findings of the present study provide new insights into the oncogenic role of OTUD7B in breast cancer and indicate that OTUD7B may serve as a therapeutic target for breast cancer.
01 Mar 2024Journal of environmental sciences (China)
Perfluorinated iodine alkanes promote the differentiation of mouse embryonic stem cells by regulating estrogen receptor signaling.
Article
Author: Zhihua Ren ; Xiaoxi Yang ; Tingting Ku ; Qian S Liu ; Jiefeng Liang ; Qunfang Zhou ; Francesco Faiola ; Guibin Jiang
Investigating the development toxicity of perfluorinated iodine alkanes (PFIs) is critical, given their estrogenic effects through binding with estrogen receptors (ERs). In the present study, two PFIs, including dodecafluoro-1,6-diiodohexane (PFHxDI) and tridecafluorohexyl iodide (PFHxI), with binding preference to ERα and ERβ, respectively, were selected to evaluate their effects on proliferation and differentiation of the mouse embryonic stem cells (mESCs). The results revealed that, similar to E2, 50 µmol/L PFHxDI accelerated the cell proliferation of the mESCs. The PFI stimulation at the exposure concentrations of 2-50 µmol/L promoted the differentiation of the mESCs as characterized by the upregulation of differentiation-related biomarkers (i.e., Otx2 and Dnmt3β) and downregulation of pluripotency genes (i.e., Oct4, Nanog, Sox2, Prdm14 and Rex1). Comparatively, PFHxDI exhibited higher induction effect on the differentiation of the mESCs than did PFHxI. The tests on ER signaling indicated that both PFI compounds induced exposure concentration-dependent expressions of ER signaling-related biomarkers (i.e., ERα, ERβ and Caveolin-1) in the mESCs, and the downstream ER responsive genes (i.e., c-fos, c-myc and c-jun) well responded to PFHxI stimulation. The role of ER in PFI-induced effects on the mESCs was further validated by the antagonistic experiments using an ER inhibitor (ICI). The findings demonstrated that PFIs triggered ER signaling, and perturbed the differentiation program of the mESCs, causing the potential health risk during early stage of development.
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