Functional genomics reveals a BMP-driven mesenchymal-to-epithelial transition in the initiation of somatic cell reprogramming.

By Payman Samavarchi-Tehrani, Azadeh Golipour, L. David, H. Sung, T. A. Beyer, A. Datti, K. Woltjen, A. Nagy, Jeffrey L. Wrana. Cell Stem Cell, 2010

1,028 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/be9765ee5943ac58331ed53db81995976ca6408f

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Citations in the corpus

Induced pluripotency: history, mechanisms, and applications. (2010, background): “…signal inhibition might be partly explained by facilitating the activation of the Nanog locus (Ichida et al. 2009), another interpretation is that blocking TGFb signaling might be critical to initiate a MET that occurs early during reprogramming (Li et al. 2010; Samavarchi-Tehrani et al. 2010).”
Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “In the embryo, multiple rounds of EMT and MET are necessary to complete gastrulation and primitive streak formation, highlighting the reversibility of this process (16).”
EMT and tumor metastasis (2015, background): “Interestingly, the miR-205 and miR-200 family of miRNAs were involved in this induction process [128].”
Facilitators and Impediments of the Pluripotency Reprogramming Factors’ Initial Engagement with the Genome (2012, positive): “The factors did not target NANOG and DPPA4, which are activated late in reprogramming (Tables S2 and S3) (Mikkelsen et al., 2008; Samavarchi-Tehrani et al., 2010; Sridharan et al., 2009).”
Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis (2015, background): “Importantly, EMT and MET, whether in physiological or pathological contexts, are not binary processes (5, 6).”
Single-cell expression analyses during cellular reprogramming reveal an early stochastic and a late hierarchic phase. (2012, background): “Recently, gene expression profiling and RNAi screening in fibroblasts revealed three phases of reprogramming termed initiation, maturation, and stabilization, with the initiation phase marked by a mesenchymal-to-epithelial transition (MET) (Li et al., 2010; Samavarchi-Tehrani et al., 2010).”
Multiple targets of miR-302 and miR-372 promote reprogramming of human fibroblasts to induced pluripotent stem cells (2011, background): “Recent work has shown that mouse fibroblasts undergo a mesenchymal-epithelial transition (MET) early in the process of reprogrammin”
Breast Cancer Stem Cells Transition between Epithelial and Mesenchymal States Reflective of their Normal Counterparts (2013, background): “However, other pathways that regulate CSCs, including those involving bone morphogenetic proteins (BMPs) and human epidermal growth factor receptor (HER) signaling, promote MET (Korkaya et al., 2012; Samavarchi-Tehrani et al., 2010).”
Epithelial Plasticity: A Common Theme in Embryonic and Cancer Cells (2013, background): “BMP7 counteracts TGFb signaling and is the most prominent known epithelializing agent, with examples seen during kidney development (35), during reprogramming of fibroblasts to induced pluripotent stem cells (iPSCs) (36), in mouse models of renal fibrosis (37), and in cancer cells (38).”
Somatic cell reprogramming and transitions between pluripotent states: facts, hypotheses, unresolved issues (2010, neutral): “In addition, a recent gene expression analysis of secondary populations of mouse embryonic fibroblasts indicated that irreversible commitment to reprogramming coincides with endogenous activation of Nanog (Samavarchi-Tehrani et al., 2010).”
Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “inducing Nanog in mouse cells, it may also promote the mesenchymal-to-epithelial transition, which is required in the early stages of reprogramming of mouse and human fibroblasts to iPS cells (Li et al., 2010; Samavarchi-Tehrani et al., 2010).”