Roles of Src Family Kinase, Ras, and mTOR Signaling in Intestinal Epithelial Homeostasis and Tumorigenesis

Dysregulation of intestinal epithelial cells(IEC) homeostasis likely contributes to the development of intestinal inflammation and intestinal cancer. The roles of receptor protein tyrosine kinases and their downstream signaling molecules such as Src family kinases, Ras, and mammalian target of rapamycin in homeostatic regulation of IEC turnover have recently been evaluated.
[Cancer Science]
Matozaki, T., Kotani, T., Murata, Y., & Saito, Y. (n.d.). Roles of Src family kinase, Ras, and mTOR signaling in intestinal epithelial homeostasis and tumorigenesis. Cancer Science, n/a(n/a). https://doi.org/10.1111/cas.14702 Cite
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IL-22 Receptor Signaling in Paneth Cells Is Critical for Their Maturation, Microbiota Colonization, Th17-Related Immune Responses, and Anti-Salmonella Immunity

Using novel Paneth cell-specific IL-22Ra1 knockout mice, researchers showed that IL-22 signaling in Paneth cells was required for small intestinal host defense. They showed that Paneth cell maturation, antimicrobial effector function, expression of specific WNTs, and organoid morphogenesis were dependent on cell-intrinsic IL-22Ra1 signaling.
[Mucosal Immunology]
Gaudino, S. J., Beaupre, M., Lin, X., Joshi, P., Rathi, S., McLaughlin, P. A., Kempen, C., Mehta, N., Eskiocak, O., Yueh, B., Blumberg, R. S., van der Velden, A. W. M., Shroyer, K. R., Bialkowska, A. B., Beyaz, S., & Kumar, P. (2020). IL-22 receptor signaling in Paneth cells is critical for their maturation, microbiota colonization, Th17-related immune responses, and anti- Salmonella immunity. Mucosal Immunology, 1–13. https://doi.org/10.1038/s41385-020-00348-5 Cite
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TAp63α Targeting of Lgr5 Mediates Colorectal Cancer Stem Cell Properties and Sulforaphane Inhibition

Researchers investigated the role of TAp63α in colorectal cancer stem cells and the effects of sulforaphane on TAp63α. They found that TAp63α was upregulated in spheres with stem cell properties compared to the parental cells.
[Oncogenesis]
Chen, Y., Wang, M., Zhu, J., Xie, C., Li, X., Wu, J., Geng, S., Han, H., & Zhong, C. (2020). TAp63α targeting of Lgr5 mediates colorectal cancer stem cell properties and sulforaphane inhibition. Oncogenesis, 9(10), 1–11. https://doi.org/10.1038/s41389-020-00273-z Cite
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Long-Term Helicobacter pylori Infection Switches Gastric Epithelium Reprogramming Towards Cancer Stem Cell-Related Differentiation Program in Hp-Activated Gastric Fibroblast-TGFβ Dependent Manner

TGFβ1 rich secretome from Helicobacter pylori-reprogrammed fibroblasts prompted phenotypic plasticity and epithelial–mesenchymal transition (EMT) of gastric epithelium, inducing pro-neoplastic expansion of post-EMT cells in the presence of low TGFβR1 and TGFβR2 activity.
[Microorganisms]
Krzysiek-Maczka, G., Targosz, A., Szczyrk, U., Wrobel, T., Strzalka, M., Brzozowski, T., Czyz, J., & Ptak-Belowska, A. (2020). Long-Term Helicobacter pylori Infection Switches Gastric Epithelium Reprogramming Towards Cancer Stem Cell-Related Differentiation Program in Hp-Activated Gastric Fibroblast-TGFβ Dependent Manner. Microorganisms, 8(10), 1519. https://doi.org/10.3390/microorganisms8101519 Cite
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LGR5 Constitutively Activates NF-κB Signaling to Regulate the Growth of Intestinal Crypts

In small intestinal crypt organoids, overexpression of a C-terminal deletion mutant of LGR5 inhibited the growth and bud formation of organoids, whereas overexpression of the R-spondin-binding mutant of LGR5 that was defective for WNT signaling could still promote organoid growth.
[FASEB Journal]
Lai, S., Cheng, R., Gao, D., Chen, Y.-G., & Deng, C. (n.d.). LGR5 constitutively activates NF-κB signaling to regulate the growth of intestinal crypts. The FASEB Journal, n/a(n/a). https://doi.org/10.1096/fj.202001329R Cite
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LGR5 Constitutively Activates NF‐κB Signaling to Regulate the Growth of Intestinal Crypts

Scientists suggest that LGR5/4‐induced NF‐κB signaling and WNT signaling may co‐regulate the growth of LGR5+ adult stem cells and intestinal crypts.
[FASEB Journal]
Lai, S., Cheng, R., Gao, D., Chen, Y.-G., & Deng, C. (n.d.). LGR5 constitutively activates NF-κB signaling to regulate the growth of intestinal crypts. The FASEB Journal, n/a(n/a). https://doi.org/10.1096/fj.202001329R Cite
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DCLK1, a Putative Novel Stem Cell Marker in Human Cholangiocarcinoma

Investigators evaluated in vitro the expression and the biological function of DCLK1 in intrahepatic cholangiocarcinom (CCA) and perihilar CCA.
[Hepatology]
Nevi, L., Matteo, S. D., Carpino, G., Zizzari, I., Safarikia, S., Ambrosino, V., Costantini, D., Overi, D., Giancotti, A., Monti, M., Bosco, D., Peppo, V. D., Oddi, A., Rose, A. M. D., Melandro, F., Bragazzi, M. C., Faccioli, J., Massironi, S., Grazi, G. L., … Alvaro, D. (n.d.). DCLK1, a putative novel stem cell marker in human cholangiocarcinoma. Hepatology, n/a(n/a). https://doi.org/10.1002/hep.31571 Cite
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An Unanticipated Tumor-Suppressive Role of the SUMO Pathway in the Intestine Unveiled by Ubc9 Haploinsufficiency

While Ubc9+/− mice displayed no overt phenotypes and no globally visible hyposumoylation in cells of the small intestine, scientists found that, upon loss of Apc in both models, Ubc9+/− mice developed more intestinal adenomas and showed significantly shortened survival. This was accompanied by reduced global sumoylation levels in the polyps, indicating that Ubc9 levels became critical upon oncogenic stress.
[Oncogene]
An unanticipated tumor-suppressive role of the SUMO pathway in the intestine unveiled by Ubc9 haploinsufficiency | Oncogene. (n.d.). Retrieved September 18, 2020, from https://www.nature.com/articles/s41388-020-01457-y Cite
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Procyanidin B2 Promotes Intestinal Injury Repair and Attenuates Colitis-Associated Tumorigenesis via Suppression of Oxidative Stress in Mouse

Scientists showed that procyanidin B2 could repress oxidative stress via nuclear factor-erythroid 2-related factor 2/ARE signaling and then promote intestine injury repair.
[Antioxidants & Redox Signaling]
Procyanidin B2 promotes intestinal injury repair and attenuates colitis-associated tumorigenesis via suppression of oxidative stress in mouse | Antioxidants & Redox Signaling. (n.d.). Retrieved September 18, 2020, from https://www.liebertpub.com/doi/10.1089/ars.2019.7911 Cite
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Non-Canonical Fzd7 Signaling Contributes to Breast Cancer Mesenchymal-Like Stemness Involving Col6a1

Frizzled-7 (Fzd7) knockdown in mesenchymal-like MDA-MB-231 and Hs578T cells reduced expression of vimentin, slug, and zinc finger E-box-binding homeobox 1, induced an epithelial-like morphology, inhibited cell motility, impaired mammosphere formation and decreased leucine-rich repeat-containing G protein-coupled receptor 5+ subpopulation.
[Cell Communication and Signaling]
Yin, P., Bai, Y., Wang, Z., Sun, Y., Gao, J., Na, L., Zhang, Z., Wang, W., & Zhao, C. (2020). Non-canonical Fzd7 signaling contributes to breast cancer mesenchymal-like stemness involving Col6a1. Cell Communication and Signaling, 18(1), 143. https://doi.org/10.1186/s12964-020-00646-2 Cite
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SMOC2, an Intestinal Stem Cell Marker, Is an Independent Prognostic Marker Associated with Better Survival in Colorectal Cancers

Investigators showed that SPARC-related modular calcium-binding protein 2 transcript level was higher in colorectal cancer samples than in normal mucosa; this level was not associated with candidate cancer stem cell markers or intestinal stem cell markers except for OLFM4.
[Scientific Reports]
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