Oncogenic BRAF, Unrestrained by TGFβ-Receptor Signaling, Drives Right-Sided Colonic Tumorigenesis

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.
[Nature Communications]
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αSMA+ Fibroblasts Suppress Lgr5+ Cancer Stem Cells and Restrain Colorectal Cancer Progression

Scientists demonstrated that αSMA+ cancer-associated fibroblast in colorectal cancer (CRC) exert tumor-restraining functions via BMP4/TGFβ1 paracrine signaling that served to suppress Lgr5+ CSCs and promoted anti-tumor immunity, ultimately limiting CRC progression.
[Oncogene]
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Vitamin D3 Suppresses Intestinal Epithelial Stemness via ER Stress Induction in Intestinal Organoids

Intestinal organoids derived from mouse small intestine were treated with vitamin D3, and the effects on intestinal stemness and differentiation were evaluated using real-time PCR and immunofluorescence staining of the distinct lineage markers.
[Stem Cell Research & Therapy]
Sittipo, P., Kim, H. K., Han, J., Lee, M. R., & Lee, Y. K. (2021). Vitamin D3 suppresses intestinal epithelial stemness via ER stress induction in intestinal organoids. Stem Cell Research & Therapy, 12(1), 285. https://doi.org/10.1186/s13287-021-02361-2 Cite
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ID4 Predicts Poor Prognosis and Promotes BDNF-Mediated Oncogenesis of Colorectal Cancer

The expression of Inhibitor of DNA binding and cell differentiation 4 (ID4), but not other ID family proteins, was enriched in LGR5-high colon cancer stem cells.
[Carcinogenesis]
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LINGO3 Regulates Mucosal Tissue Regeneration and Promotes TFF2 Dependent Recovery from Colitis

The authors found that LINGO3 was broadly expressed on human enterocytes and sparsely on discrete cells within the crypt niche, that contained sintestinal stem cells.
[Scandinavian Journal of Gastroenterology]
Zullo, K. M., Douglas, B., Maloney, N. M., Ji, Y., Wei, Y., Herbine, K., Cohen, R., Pastore, C., Cramer, Z., Wang, X., Wei, W., Somsouk, M., Hung, L. Y., Lengner, C., Kohanski, M. H., Cohen, N. A., & Herbert, D. R. (2021). LINGO3 regulates mucosal tissue regeneration and promotes TFF2 dependent recovery from colitis. Scandinavian Journal of Gastroenterology, 0(0), 1–15. https://doi.org/10.1080/00365521.2021.1917650 Cite
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The ZMYND8-Regulated Mevalonate Pathway Endows YAP-High Intestinal Cancer with Metabolic Vulnerability

Disruption of the ZMYND8-dependent MVA pathway greatly restricted the self-renewal capacity of Lgr5+ intestinal stem cells and intestinal tumorigenesis.
[Molecular Cell]
Pan, Q., Zhong, S., Wang, H., Wang, X., Li, N., Li, Y., Zhang, G., Yuan, H., Lian, Y., Chen, Q., Han, Y., Guo, J., Liu, Q., Qiu, T., Jiang, J., Li, Q., Tan, M., Yin, H., Peng, J., … Qin, J. (2021). The ZMYND8-regulated mevalonate pathway endows YAP-high intestinal cancer with metabolic vulnerability. Molecular Cell, 0(0). https://doi.org/10.1016/j.molcel.2021.04.009 Cite
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mTOR Signaling Regulates Gastric Epithelial Progenitor Homeostasis and Gastric Tumorigenesis via MEK1-ERKs and BMP-Smad1 Pathways

Scientists provide genetic evidence that mTOR activation promotes proliferation and inhibits differentiation of Lgr5+ gastric epithelial progenitors in gastric homeostasis and tumorigenesis.
[Cell Reports]
Li, K., Wu, H., Wang, A., Charron, J., Mishina, Y., Habib, S. L., Liu, H., & Li, B. (2021). mTOR signaling regulates gastric epithelial progenitor homeostasis and gastric tumorigenesis via MEK1-ERKs and BMP-Smad1 pathways. Cell Reports, 35(5). https://doi.org/10.1016/j.celrep.2021.109069 Cite
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Non-Muscle Myosin Heavy Chain 9 Maintains Intestinal Homeostasis by Preventing Epithelium Necroptosis and Colitis Adenoma Formation

Myh9 deletion disturbs cell junctions and impairs intestinal lumen barrier integrity, promoting the necroptosis of epithelial cells.
[Stem Cell Reports]
Wang, S., Li, S., Li, Y., Jiang, Q., Li, X., Wang, Y., Han, J.-D., Liu, Y., & Chen, Y.-G. (2021). Non-muscle myosin heavy chain 9 maintains intestinal homeostasis by preventing epithelium necroptosis and colitis adenoma formation. Stem Cell Reports, 0(0). https://doi.org/10.1016/j.stemcr.2021.03.027 Cite
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HER2 and APC Mutations Promote Altered Crypt-Villus Morphology and Marked Hyperplasia in the Intestinal Epithelium

Investigators analyzed Lgr5-Cre; APCmin; HER2V777LTg mice by morphologic and gene expression assays on intestinal sections and organoids derived from the epithelium.
[Cellular and Molecular Gastroenterology and Hepatology]
Murray, E., Cheng, X., Krishna, A., Jin, X., Ohara, T. E., Stappenbeck, T. S., & Bose, R. (2021). HER2 and APC mutations promote altered crypt-villus morphology and marked hyperplasia in the intestinal epithelium. Cellular and Molecular Gastroenterology and Hepatology. https://doi.org/10.1016/j.jcmgh.2021.04.012 Cite
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Dickkopf-2 Regulates the Stem Cell Marker LGR5 in Colorectal Cancer via HNF4α1

Scientists report a Wnt ligand, Dickkopf-2 (DKK2) was essential for developing colorectal cancer stemness. Genetic depletion of Dkk2 in intestinal epithelial or stem cells reduced tumorigenesis as well as expression of the stem cell marker genes including Lgr5 in a model of colitis-associated cancer.
[iScience]
Shin, J. H., Jeong, J., Choi, J., Lim, J., Dinesh, R. K., Braverman, J., Hong, J. Y., Maher, S. E., Vesely, M. C. A., Kim, W., Koo, J.-H., Tang, W., Wu, D., Blackburn, H. N., Xicola, R. M., Llor, X., Yilmaz, O., Choi, J.-M., & Bothwell, A. L. M. (2021). Dickkopf-2 regulates the stem cell marker LGR5 in colorectal cancer via HNF4α1. IScience, 0(0). https://doi.org/10.1016/j.isci.2021.102411 Cite
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Silencing PTEN in the Fallopian Tube Promotes Enrichment of Cancer Stem Cell-Like Function through Loss of PAX2

Loss of PTEN in fallopian tube epithelium led to the enrichment of CSC markers such as LGR5, WNT4, ALDH1, CD44.
[Cell Death & Disease]
Russo, A., Colina, J. A., Moy, J., Baligod, S., Czarnecki, A. A., Varughese, P., Lantvit, D. D., Dean, M. J., & Burdette, J. E. (2021). Silencing PTEN in the fallopian tube promotes enrichment of cancer stem cell-like function through loss of PAX2. Cell Death & Disease, 12(4), 1–14. https://doi.org/10.1038/s41419-021-03663-2 Cite
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