Researchers showed that restricted chromatin accessibility in intestinal stem cells prevented the expression of β-Catenin-regulated metabolic enzymes, whereas fine-tuning of WNT/β-Catenin activity by ZNRF3 and RNF43 restricted proliferation in chromatin-permissive AXIN2+ hepatocytes, while preserving metabolic function.
[Cell Stem Cell]
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Sun, T., Annunziato, S., Bergling, S., Sheng, C., Orsini, V., Forcella, P., Pikiolek, M., Kancherla, V., Holwerda, S., Imanci, D., Wu, F., Meylan, L. C., Puehringer, L. F., Waldt, A., Oertli, M., Schuierer, S., Terracciano, L. M., Reinker, S., Ruffner, H., … Tchorz, J. S. (2021). ZNRF3 and RNF43 cooperate to safeguard metabolic liver zonation and hepatocyte proliferation. Cell Stem Cell, 0(0). https://doi.org/10.1016/j.stem.2021.05.013 Cite
Researchers employed a doxycycline-inducible phosphatase of regenerating liver-3 (PRL-3) mouse strain to show that aberrant PRL-3 expression within a non-cancerous background led to the death of Lgr5+ intestinal stem cells and to Paneth cell expansion.
[Journal of Molecular Medicine]
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By targeting antiapoptotic proteins with specific BH3 mimetics in organoid models of colorectal cancer progression, scientists found that BCL-2 was essential only during instestinal stem cell transformation while MCL1 inhibition did not affect adenoma outgrowth.
[Cell Death & Differentiation]
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The proximal colonic tumors that developed in a mouse model of right-sided colon cancer exhibited a fetal-like progenitor phenotype (Ly6a/Sca1+) and lacked expression of Lgr5 and its associated intestinal stem cell signature.
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Scientists proposed that a high-fat diet enhanced intestinal stemness and tumorigenicity by engaging a peroxisome proliferator-activated receptor-fatty acid oxidation (PPAR-FAO) program.
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In addition to impacting stem cell proliferation during damage-induced intestinal regeneration, the role of RAL GTPases impacted on EGFR-dependent tumorigenic growth in the intestine and in human mammary epithelium.
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Investigators showed that Apc-mutant intestinal stem cells (ISCs) functioned as bona fide supercompetitors by secreting WNT antagonists, thereby inducing differentiation of neighbouring wild-type ISCs.
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van Neerven, S. M., de Groot, N. E., Nijman, L. E., Scicluna, B. P., van Driel, M. S., Lecca, M. C., Warmerdam, D. O., Kakkar, V., Moreno, L. F., Vieira Braga, F. A., Sanches, D. R., Ramesh, P., ten Hoorn, S., Aelvoet, A. S., van Boxel, M. F., Koens, L., Krawczyk, P. M., Koster, J., Dekker, E., … Vermeulen, L. (2021). Apc-mutant cells act as supercompetitors in intestinal tumour initiation. Nature, 1–6. https://doi.org/10.1038/s41586-021-03558-4 Cite
Researchers investigated how Apc-mutant cells gain a clonal advantage over wild-type counterparts to achieve fixation and found that Apc-mutant cells were enriched for transcripts that encoded several secreted WNT antagonists, with Notum being the most highly expressed.
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Cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) deficiency led to intestinal stem cell loss and compromised intestinal barrier integrity upon dextran sodium sulfate-induced acute injury.
[Proceedings of the National Academy of Sciences of the United States of America]
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Following successful research that showed how a drug available on the NHS could boost fitness of healthy stem cells in the gut, a clinical trial funded by the Dutch Cancer Society testing the effect of lithium of bowel cancer development in individuals with familial adenomatous polyposis will be performed in the Netherlands.
[Worldwide Cancer Research (EurekAlert!)]
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Investigators provided a detailed protocol for an autologous in vitro long-term 3D co-culture system of human intestinal CD4+ T cells and intestinal stem cells to study T cell-intestinal epithelial cell interactions during tissue development and inflammation.