scholarly journals The reactivation of reprogramming factors within human blastocysts by using ATP contribute to human blastocyst development

2017 ◽  
Author(s):  
Takashi Takemura ◽  
Midori Okabe
Keyword(s):  
Transcription Factor ◽  
Disodium Salt ◽  
The Other ◽  
Blastocyst Development ◽  
Salt Hydrate ◽  
Pou Domain ◽  
Human Blastocyst ◽  
Mouse Hepatocytes ◽  
Reprogramming Factors ◽  
Transcription Factor 1

AbstractScientists worldwide have been unable to replicate the stimulus-triggered acquisition of pluripotency (STAP) cells and/or the STAP phenomenon. However, investigations into STAP cells and/or the STAP phenomenon by RIKEN CDB in Japan found that ATP (adenosine 5’-triphosphate disodium salt hydrate) can upregulate Oct3/4 (POU5F1: POU domain, class 5, transcription factor 1) and Nanog mRNA expression in mouse hepatocytes.On the other hand, no studies have investigated whether ATP can contribute to human blastocyst development. Here we show the reactivation of reprogramming factors within human blastocysts by appropriate ATP treatment (1 mM for 2 days) can contribute to human blastocyst development.In conclusion, although ATP treatment could not replicate STAP cells and/or the STAP phenomenon by scientists worldwide, appropriate ATP treatment (1 mM for 2 days) in cultured human blastocysts with totipotency would be helpful for infertility women.

scholarly journals BRN2 is a non-canonical melanoma tumor-suppressor

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Michael Hamm ◽  
Pierre Sohier ◽  
Valérie Petit ◽  
Jérémy H. Raymond ◽  
Véronique Delmas ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Tumor Suppressor ◽  
The Other ◽  
Pi3k Signaling ◽  
Melanoma Tumor ◽  
Temporal Regulation ◽  
Metastatic Colonization ◽  
Pou Domain

AbstractWhile the major drivers of melanoma initiation, including activation of NRAS/BRAF and loss of PTEN or CDKN2A, have been identified, the role of key transcription factors that impose altered transcriptional states in response to deregulated signaling is not well understood. The POU domain transcription factor BRN2 is a key regulator of melanoma invasion, yet its role in melanoma initiation remains unknown. Here, in a BrafV600EPtenF/+ context, we show that BRN2 haplo-insufficiency promotes melanoma initiation and metastasis. However, metastatic colonization is less efficient in the absence of Brn2. Mechanistically, BRN2 directly induces PTEN expression and in consequence represses PI3K signaling. Moreover, MITF, a BRN2 target, represses PTEN transcription. Collectively, our results suggest that on a PTEN heterozygous background somatic deletion of one BRN2 allele and temporal regulation of the other allele elicits melanoma initiation and progression.

scholarly journals LncRNA NEAT1 Promotes Inflammatory Response in Sepsis via the miR-31-5p/POU2F1 Axis

Inflammation ◽  
2021 ◽  
Author(s):  
Yang Yang ◽  
Jianhua Xue ◽  
Lili Qin ◽  
Jiaxuan Zhang ◽  
Jiajia Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Transcription Factor ◽  
Inflammatory Response ◽  
Underlying Mechanism ◽  
Raw264.7 Cells ◽  
Potential Therapeutic Target ◽  
Pou Domain ◽  
Lncrna Neat1 ◽  
Transcription Factor 1 ◽  
Abundant Transcript

Abstract Sepsis is considered to be a systemic inflammatory response, which results in organ dysfunction. LncRNA nuclear-enriched abundant transcript 1 (NEAT1) involved in sepsis progression has been reported. However, the underlying mechanism of NEAT1 in sepsis-induced inflammatory response remains to be revealed. In this study, NEAT1 and POU domain class 2 transcription factor 1 (POU2F1) were highly expressed in LPS-induced septic RAW264.7 cells, opposite to miR-31-5p expression. Furthermore, we found that NEAT1 silencing inhibited LPS-induced inflammatory response and cell proliferation, and promoted cell apoptosis. Subsequently, we found that miR-31-5p interacted with NEAT1 and targeted the 3′UTR of POU2F1, and in LPS-induced RAW264.7 cells, the inhibition of NEAT1 silencing was reversed by miR-31-5p knockdown, while POU2F1 downregulation could cover the functions of miR-31-5p knockdown. In a word, this study indicates that NEAT1 inhibits the LPS-induced progression of sepsis in RAW264.7 cells by modulating miR-31-5p/POU2F1 axis, suggesting that NEAT1 will be the potential therapeutic target for sepsis.

scholarly journals Impact of OCT4 and Its Related Signaling Pathways on Gastrointestinal Cancers: Focusing on Targeted Therapy

2020 ◽  
Author(s):  
Hamid Cheshomi ◽  
Omid Gholami ◽  
Babak Peyroshabani ◽  
Abolfazl Rad
Keyword(s):  
Stem Cells ◽  
Transcription Factor ◽  
Cancer Stem Cells ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Gastrointestinal Cancers ◽  
Oct4 Expression ◽  
Pou Domain ◽  
Transcription Factor 4 ◽  
Transcription Factor 1

There are many pieces of evidence support the effect of cancer stem cells on the initiation and progression of cancer. However, related mechanisms involved in these phenomena are far more complicated to understand. The function of different stemness factorsin cancer stem cells (CSCs) and their complex associations at different levels of cancer have been reported. Therefore, it seems that focusing on one master factor would be more helpful to complete the puzzle of singling pathways in these cells. Octamer-binding transcription factor 4 (OCT4) also known as POU domain, class 5, transcription factor 1(POU5F1), one of these key pluripotency factors, has important roles in both embryogenesis and tumorigenesis. In this review, we gathered information about the association of different markers with OCT4 expression in three types of gastrointestinal cancers including esophageal, gastric and colorectal cancers. OCT4 through different signaling pathways has an impact on different processes of gastrointestinal cancers such as proliferation, invasion, and metastasis. Based on the literature, OCT4 has great effects on cancer progression at different stages, therefore we suggested it has potential implications in therapeutic options.

scholarly journals Oct-1 interacts with conserved motifs in the human thyroid transcription factor 1 gene minimal promoter

1996 ◽  
Vol 319 (3) ◽  
pp. 669-674 ◽  
Author(s):  
Colin D BINGLE ◽  
Sharon GOWAN
Keyword(s):  
Transcription Factor ◽  
Binding Sites ◽  
Molecular Mechanisms ◽  
Proximal Promoter ◽  
Human Thyroid ◽  
Thyroid Transcription Factor 1 ◽  
Pou Domain ◽  
Specific Distribution ◽  
Thyroid Transcription Factor ◽  
Transcription Factor 1

The homeodomain containing thyroid transcription factor 1 (TTF-1) is a lung- and thyroid-enriched protein implicated in the regulation of a number of pulmonary specific genes. Within the lung TTF-1 is expressed within the epithelial cells. Although the molecular mechanisms that govern this tight cell-type-specific distribution are unclear, transient transfection studies have suggested that tissue specificity is conferred in part by regions of the proximal promoter. Further studies have shown that two functionally important regions (BS1 and BS2) are sites for activation of the TTF-1 gene by the homeodomain protein HoxB3, raising the possibility that Hox proteins might function in the regulation of TTF-1 in vivo. The different cellular distributions of the two proteins within the lung suggest, however, that proteins distinct from HoxB3 might be the mediators of expression through these sites. In the present study we have used gel-mobility-shift experiments to show that in a pulmonary adenocarcinoma cell line (NCI-H441) that expresses TTF-1, the same single protein binds to both of these sites. The binding of this protein is competed for specifically by the addition of oligonucleotides containing a range of octamer-binding sites but not by a variety of non-related binding sites. Using specific antiserum we have identified this protein as being the ubiquitously expressed POU-domain protein Oct-1. Reverse transcriptase-PCR performed with degenerated primers suggests that Oct-1 is the major POU-domain-containing protein expressed in H441 cells. These results suggest that BS1 and BS2 are functional octamer sites and might therefore be implicated in the basal rather than the tissue-restricted expression of the TTF-1 gene.

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