PubMed DB- Latest Entries for Mesenchymal Stem Cells
PubMed DB- Latest Entries for Mesenchymal Stem Cells

PubMed- Latest Free Papers on MSCs

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PubMed comprises more than 26 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites. 

The query  I made on PubMed for this section of the page, was Free Papers  AND on "Mesenchymal + Stromal + Cells". The outcome thereof  (10 returns) you will find below- of course, during the course of time, this RSS feed most likely will look different all the time- and that is of course the purpose and genial thing about RSS feeds- you always get the latest and most current stuff..

 

 

pubmed: mesenchymal stem cel...

NCBI: db=pubmed; Term=mesenchymal stem cells AND (free full text[sb])
  • Telomerase reverse transcriptase coordinates with the epithelial-to-mesenchymal transition through a feedback loop to define properties of breast cancer stem cells.
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    Telomerase reverse transcriptase coordinates with the epithelial-to-mesenchymal transition through a feedback loop to define properties of breast cancer stem cells.

    Biol Open. 2018 Jun 15;:

    Authors: El-Badawy A, Ghoneim NI, Nasr MA, Elkhenany H, Ahmed TA, Ahmed SM, El-Badri N

    Abstract
    Telomerase and its core component, telomerase reverse transcriptase (hTERT), are critical for stem cell compartment integrity. Normal adult stem cells have the longest telomeres in a given tissue, a property mediated by high hTERT expression and high telomerase enzymatic activity. In contrast, cancer stem cells (CSCs) have short telomeres despite high expression of hTERT, indicating that the role of hTERT in CSCs is not limited to telomere elongation and/or maintenance. The function of hTERT in CSCs remains poorly understood. Here, we knocked down hTERT expression in CSCs and observed a morphological shift to a more epithelial phenotype, suggesting a role for hTERT in the epithelial-to-mesenchymal transition (EMT) of CSCs. Therefore, in this study, we systematically explored the relationship between hTERT and EMT and identified a reciprocal, bidirectional feedback loop between hTERT and EMT in CSCs. We found that hTERT expression is mutually exclusive to the mesenchymal phenotype and that, reciprocally, loss of the mesenchymal phenotype represses hTERT expression. We also showed that hTERT plays a critical role in the expression of key CSC markers and nuclear β-catenin localization, increases the percentage of cells with side-population properties, and upregulates the CD133 expression. hTERT also promotes chemoresistance properties, tumorsphere formation and other important functional CSC properties. Subsequently, hTERT knockdown leads to the loss of the above advantages, indicating a loss of CSC properties. Our findings suggest that targeting hTERT might improve CSCs elimination by transitioning them from the aggressive mesenchymal state to a more steady epithelial state, thereby preventing cancer progression.

    PMID: 29907642 [PubMed - as supplied by publisher]

  • Arginine methylation of Smad7 by PRMT1 in TGF-β-induced epithelial-mesenchymal transition and epithelial stem cell generation.
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    Arginine methylation of Smad7 by PRMT1 in TGF-β-induced epithelial-mesenchymal transition and epithelial stem cell generation.

    J Biol Chem. 2018 Jun 15;:

    Authors: Katsuno Y, Qin J, Oses-Prieto JA, Wang H, Jackson-Weaver O, Zhang T, Lamouille S, Wu J, Burlingame ALL, Xu J, Derynck R

    Abstract
    The epithelial-to-mesenchymal transdifferentiation (EMT) is crucial for tissue differentiation in development, and drives essential steps in cancer and fibrosis. EMT is accompanied by reprogramming of gene expression, and has been associated with the epithelial stem cell state in normal and carcinoma cells. The cytokine TGF-β drives this program in cooperation with other signaling pathways and through TGF-β-activated Smad3 as major effector. TGF-β-induced Smad3 activation is inhibited by Smad7 and to a lesser extent by Smad6, and Smad6 and Smad7 both inhibit Smad1 and Smad5 activation in response to the TGF-β-related bone morphogenetic proteins (BMPs). We previously reported that, in response to BMP, the protein arginine methyltransferase PRMT1 methylates Smad6 at the BMP receptor complex, thereby promoting its dissociation from the receptors and enabling BMP-induced Smad1 and Smad5 activation. We now provide evidence that PRMT1 also facilitates TGF-β signaling by methylating Smad7, which complements Smad6 methylation. We found that PRMT1 is required for TGF-β-induced Smad3 activation, through a mechanism similar to that of BMP-induced Smad6 methylation, and thus promotes the TGF-β-induced EMT and epithelial stem cell generation. This critical mechanism positions PRMT1 as an essential mediator of TGF-β signaling that controls the EMT and epithelial cell stemness through Smad7 methylation.

    PMID: 29907569 [PubMed - as supplied by publisher]

 

 

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