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myc, cells, lef, expression, wnt, cancer, cell, pubmed, fig, pathway, genes, article, colon, additional, scholar, google, cas, levels, control, file, βcatenin, figure, mycexpressing, human, activity, nuclear, western, signaling, expressing, rat, knockdown, transfected, dld, central, activation, blotting, apc, fibroblasts, acad, transcription, sirna, performed, pparδ, days, icg, vector, found, normal, gene, samples,

Topics {✒️}

beta-catenin/tcf-coordinated chromatin loop helix-loop-helix zipper protein β-catenin-related protein β-catenin kaplan–meier survival curves canonical wnt/beta-catenin pathway antagonizes wnt signalling myc-driven wnt-related genes sequence-specific dna-binding complex tcf/lef transcription factors article download pdf maralice conacci-sorrell long-chain fatty acid 50 mm tris-hcl ph 7 myc-dependent wnt-related genes intracellular tcf/lef composition lymphoid enhancer factor-1 colon cancer-related alterations beta-catenin nuclear dynamics beta-catenin/lef-1 pathway beta-catenin-tcf complex beta-catenin destruction complex myc-related gene amplified somatic copy-number alteration wnt/beta-catenin signaling β-catenin-tcf/lef nonparametric kruskal-wallis test nonsteroidal anti-inflammatory drugs noncanonical wnt/fz signaling tcf/lef1-mediated control wnt-related gene lef1 myc-driven colorectal tumors beta-catenin-sensitive isoforms myc-induced transcription factors numerous wnt-related genes fatty acid-regulating genes rna-seq analysis showed affect β-catenin localization tcf/lef factors hcec expressing oncogenes performed sirna-mediated knockdown myc-dependent colonic cells colon cancer formation colon cancer progression fatty acid metabolism remove low-expressed genes tcf/lef binding [27] myc-expressing cells led lef1/β-catenin complex maintains cell proliferation tcf/lef proteins

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         headline:Induction of LEF1 by MYC activates the WNT pathway and maintains cell proliferation
         description:While regulated WNT activity is required for normal development and stem cell maintenance, mutations that lead to constitutive activation of the WNT pathway cause cellular transformation and drive colorectal cancer. Activation of the WNT pathway ultimately leads to the nuclear translocation of β-catenin which, in complex with TCF/LEF factors, promotes the transcription of genes necessary for growth. The proto-oncogene MYC is one of the most critical genes activated downstream the WNT pathway in colon cancer. Here, we investigate the converse regulation of the WNT pathway by MYC. We performed RNA-seq analyses to identify genes regulated in cells expressing MYC. We validated the regulation of genes in the WNT pathway including LEF1 by MYC using RT-qPCR, Western blotting, and ChIP-seq. We investigated the importance of LEF1 for the viability of MYC-expressing cells in in fibroblasts, epithelial cells, and colon cells. Bioinformatic analyses were utilized to define the expression of MYC-regulated genes in human colon cancer and metabolomics analyses were used to identify pathways regulated by LEF1 in MYC expressing cells. MYC regulates the levels of numerous WNT-related genes, including the β-catenin co-transcription factor LEF1. MYC activates the transcription of LEF1 and is required for LEF1 expression in colon cancer cells and in primary colonic cells transformed by APC loss of function, a common mutation in colon cancer patients. LEF1 caused the retention of β-catenin in the nucleus, leading to the activation of the WNT pathway in MYC-expressing cells. Consequently, MYC-expressing cells were sensitive to LEF1 inhibition. Moreover, we describe two examples of genes induced in MYC-expressing cells that require LEF1 activity: the peroxisome proliferator activated receptor delta (PPARδ) and the Acyl CoA dehydrogenase 9 (ACAD9). We demonstrated that MYC is a transcriptional regulator of LEF1 in colonic cells. Our work proposes a novel pathway by which MYC regulates proliferation through activating LEF1 expression which in turn activates the WNT pathway.
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            Cell Biology
            Protein-Ligand Interactions
            Receptors
            Cytokines and Growth Factors
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      headline:Induction of LEF1 by MYC activates the WNT pathway and maintains cell proliferation
      description:While regulated WNT activity is required for normal development and stem cell maintenance, mutations that lead to constitutive activation of the WNT pathway cause cellular transformation and drive colorectal cancer. Activation of the WNT pathway ultimately leads to the nuclear translocation of β-catenin which, in complex with TCF/LEF factors, promotes the transcription of genes necessary for growth. The proto-oncogene MYC is one of the most critical genes activated downstream the WNT pathway in colon cancer. Here, we investigate the converse regulation of the WNT pathway by MYC. We performed RNA-seq analyses to identify genes regulated in cells expressing MYC. We validated the regulation of genes in the WNT pathway including LEF1 by MYC using RT-qPCR, Western blotting, and ChIP-seq. We investigated the importance of LEF1 for the viability of MYC-expressing cells in in fibroblasts, epithelial cells, and colon cells. Bioinformatic analyses were utilized to define the expression of MYC-regulated genes in human colon cancer and metabolomics analyses were used to identify pathways regulated by LEF1 in MYC expressing cells. MYC regulates the levels of numerous WNT-related genes, including the β-catenin co-transcription factor LEF1. MYC activates the transcription of LEF1 and is required for LEF1 expression in colon cancer cells and in primary colonic cells transformed by APC loss of function, a common mutation in colon cancer patients. LEF1 caused the retention of β-catenin in the nucleus, leading to the activation of the WNT pathway in MYC-expressing cells. Consequently, MYC-expressing cells were sensitive to LEF1 inhibition. Moreover, we describe two examples of genes induced in MYC-expressing cells that require LEF1 activity: the peroxisome proliferator activated receptor delta (PPARδ) and the Acyl CoA dehydrogenase 9 (ACAD9). We demonstrated that MYC is a transcriptional regulator of LEF1 in colonic cells. Our work proposes a novel pathway by which MYC regulates proliferation through activating LEF1 expression which in turn activates the WNT pathway.
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         WNT/β-catenin pathway
         LEF1
         Colon cancer
         Tumorigenesis
         Metabolism
         PPARδ
         ACAD9
         Proliferation
         Cell Biology
         Protein-Ligand Interactions
         Receptors
         Cytokines and Growth Factors
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      name:Department of Cell Biology, UT Southwestern Medical Center, Dallas, USA
      name:Harold C. Simmons Comprehensive Cancer Center, UT Southwestern Medical Center, Dallas, USA
      name:Hamon Center for Regenerative Science and Medicine, UT Southwestern Medical Center, Dallas, USA

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