Dual regulatory switch through interactions of Tcf7l2/Tcf4 with stage-specific partners propels oligodendroglial maturation

Zhao, Chuntao; Deng, Yaqi; Liu, Lei; Yu, Kun; Zhang, Liguo; Wang, Haibo; He, Xuelian; Wang, Jincheng; Lu, Chang; Wu, Laiman; Weng, Qinjie; Mao, Meng; Lǐ, Jiànróng; Es, Johan H. van; Xin, Mei; Parry, Lee; Goldman, Steven A.; Clevers, Hans; Lü, Qing

doi:10.1038/ncomms10883

Cited by 117 publications

(139 citation statements)

References 66 publications

(112 reference statements)

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“…Consistent with this, genome-wide surveys of TCF or β-cat binding in vertebrates reveal the presence of several TF binding site motifs besides the TCF site consensus 1, 30, 39, 77, 78 . Other TFs have been reported to co-localize with TCFs 36, 38, 39, 79, 80 , and in the cases of Cdx2 79 , Sp5/8 81 , and TEAD TFs 82 , a co-dependency with TCFs or β-cat for chromatin association has been reported. In addition, TCF binding to chromatin is highly cell type specific 36 and is dynamic over time in the same cell type 38, 39 .…”

Section: Tcfs and Wnt Target Locationsupporting

confidence: 65%

Wnt target genes and where to find them

Ramakrishnan

Cadigan

2017

F1000Res

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Wnt/β-catenin signaling is highly conserved throughout metazoans, is required for numerous essential events in development, and serves as a stem cell niche signal in many contexts. Misregulation of the pathway is linked to several human pathologies, most notably cancer. Wnt stimulation results in stabilization and nuclear import of β-catenin, which then acts as a transcriptional co-activator. Transcription factors of the T-cell family (TCF) are the best-characterized nuclear binding partners of β-catenin and mediators of Wnt gene regulation. This review provides an update on what is known about the transcriptional activation of Wnt target genes, highlighting recent work that modifies the conventional model. Wnt/β-catenin signaling regulates genes in a highly context-dependent manner, and the role of other signaling pathways and TCF co-factors in this process will be discussed. Understanding Wnt gene regulation has served to elucidate many biological roles of the pathway, and we will use examples from stem cell biology, metabolism, and evolution to illustrate some of the rich Wnt biology that has been uncovered.

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Section: Tcfs and Wnt Target Locationsupporting

confidence: 65%

Wnt target genes and where to find them

Ramakrishnan

Cadigan

2017

F1000Res

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“…Enrichment analysis identified genes relevant to myelination and axonal guidance (Table 1). Pathway analysis also highlighted Tcf7l2 , a transcription factor involved in Wnt signaling (Welters & Kulkarni, 2008) and myelination (Zhao et al ., 2016), as a top upstream regulator (Fig. 4).…”

Section: Discussionmentioning

confidence: 99%

Casein kinase 1‐epsilon deletion increases mu opioid receptor‐dependent behaviors and binge eating1

Goldberg

Kirkpatrick

Yazdani

et al. 2017

Genes Brain and Behavior

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Genetic and pharmacological studies indicate that casein kinase-1 epsilon (Csnk1e) contributes to psychostimulant, opioid, and ethanol motivated behaviors. We previously used pharmacological inhibition to demonstrate that Csnk1e negatively regulates the locomotor stimulant properties of opioids and psychostimulants. Here, we tested the hypothesis that Csnk1e negatively regulates opioid and psychostimulant reward using genetic inhibition and the conditioned place preference assay in Csnk1e knockout mice. Similar to pharmacological inhibition, Csnk1e knockout mice showed enhanced opioid-induced locomotor activity with the mu opioid receptor agonist fentanyl (0.2 mg/kg i.p.) as well as enhanced sensitivity to low-dose fentanyl reward (0.05 mg/kg). Interestingly, female knockout mice also showed a markedly greater escalation in consumption of sweetened palatable food – a behavioral pattern consistent with binge eating that also depends on mu opioid receptor activation. No difference was observed in fentanyl analgesia in the 52.5°C hot plate assay (0–0.4 mg/kg), naloxone conditioned place aversion (4 mg/kg), or methamphetamine conditioned place preference (0–4 mg/kg). To identify molecular adaptations associated with increased drug and food behaviors in knockout mice, we completed transcriptome analysis via mRNA sequencing of the striatum. Enrichment analysis identified terms associated with myelination and axon guidance and pathway analysis identified a differentially expressed gene set predicted to be regulated by the Wnt signaling transcription factor, Tcf7l2. To summarize, Csnk1e deletion increased mu opioid receptor-dependent behaviors, supporting previous studies indicating an endogenous negative regulatory role of Csnk1e in opioid behavior.

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“…The transcription factor 7-like 2 (TCF7L2) gene, previously called TCF-4, may affect cancer progression because the TCF7L2 gene product is involved in the Wnt/β-catenin signaling pathway [42]. Dysregulation of the Wnt/β-catenin pathway and TCF target genes plays a role in carcinogenesis and is especially well documented for colorectal cancer [43-46].…”

Section: Discussionmentioning

confidence: 99%

The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

et al. 2017

Cell Physiol Biochem

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Background/Aims: The long non-coding RNA colorectal neoplasia differentially expressed (CRNDE) contributes to the proliferation and migration of tumors. However, its molecular mechanism underlying gastric cancer remains unknown. In the present study, we investigated whether CRNDE was involved in the development of colorectal cancer via the binding of microRNA (miR)-217 with transcription factor 7-like 2 (TCF7L2) to enhance the Wnt signaling pathway. Methods: Quantitative polymerase chain reaction was used to detect CRNDE, miR-217 and TCF7L2 in colorectal cancer tissues and cells. The CCK-8 assay, wound healing assay, and Transwell assay were used to detect cell proliferation, migration and invasion, respectively. Western blotting and luciferase activity assays were used to identify CRNDE and TCF7L2 as one of the direct targets of miR-217. The activity of the Wnt/β-catenin signaling pathway was analyzed by the TOPflash assay, and the subcellular localization of β-catenin and TCF7L2 was analyzed by western blotting and confocal microscopy. Results: In this study, we found that high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells. The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression. CRNDE down-regulation inhibited the cell proliferation, migration and invasion in vitro and in vivo and the inhibitions were both completely blocked after miR-217 inhibition or TCF7L2 overexpression. Finally, TOPflash analysis showed that the activity of Wnt/β-catenin signaling is inhibited by CRNDE down-regulation and rescued by TCF7L2 over-expression. Consistently immunostaining and western blotting analysis showed that the expression of b-catenin and TCF7L2 in the nucleus was significantly decreased by CRNDE down-regulation and was rescued by TCF7L2 over-expression. Conclusions: The present study suggest that CRNDE involves in the cell proliferation, migration and invasion of colorectal cancer cells via increasing the expression of TCF7L2 and activity of Wnt/β-catenin signaling through binding miR-217 competitively.

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Dual regulatory switch through interactions of Tcf7l2/Tcf4 with stage-specific partners propels oligodendroglial maturation

Cited by 117 publications

References 66 publications

Wnt target genes and where to find them

Wnt target genes and where to find them

Casein kinase 1‐epsilon deletion increases mu opioid receptor‐dependent behaviors and binge eating1

The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

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