 | | Vol. 6.36 – 18 September, 2020 |
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| By using tissue engineering and the intrinsic self-organization properties of cells, researchers induced intestinal stem cells to form tube-shaped epithelia with an accessible lumen and a similar spatial arrangement of crypt-and villus-like domains to that in vivo.
[Nature] |
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 | | PUBLICATIONSRanked by the impact factor of the journal |
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| ApcMin/+ mice were given intraperitoneal injection of adeno-associated viral vector encoding an RSPO1–Fc fusion protein or a control vector. Intestinal crypts were isolated from ApcMin/+ mice and cultured as organoids, which were incubated with or without RSPO1–Fc and an inhibitor of transforming growth factor beta receptor.
[Gastroenterology] |
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| Researchers demonstrated that RNF43 mutations cooperated with KRAS mutations to promote multi-step tumorigenesis via the Wnt-Ras-p53 axis in human colon cancers. Phosphomimetic substitutions of the serine trio restored the tumour suppressive activity of extracellular oncogenic mutants.
[Nature Communications] |
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| The authors showed that Lsd1-deficient crypts, devoid of paneth cells, were still able to form organoids without a requirement of exogenous or endogenous Wnt. They found that LSD1 enzymatically repressed genes that were normally expressed only in fetal and neonatal epithelium.
[Science Advances] |
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| 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] |
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| 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] |
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| Investigators found that HDAC3 regulated B7x transcription by promoting the binding of the transcription activator C/EBP-α with the B7x promoter region. Their data indicated that an antibody neutralizing B7x augmented the response to HDAC inhibitor in the colorectal cancer xenograft model and the lung metastasis model by increasing the ratios of both CD4-positive and CD8-positive T cells.
[Cell Death & Disease] |
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| Researchers showed that matrix metalloproteinase 9 expression correlated with the reduced reactive oxygen species levels, decreased DNA damage, and upregulated mismatch repair pathway.
[Cell Death & Disease] |
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| Lewisx, Sox2, ALDH and CD44 expression, tumorsphere formation, resistance to 5-FU treatment and in vivo tumor growth were increased in FUT9-expressing MC38 cells compared to the control cells. Likewise, human CRC cell lines highly expressing FUT9 displayed phenotypic features of cancer stem cells, which were significantly impaired upon FUT9 knock-out.
[Cancers] |
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| The authors inventory the genes involved in the lack of colorectal cancer response to pharmacological treatment, classifying them into seven groups according to functional criteria to identify cancer cell weaknesses.
[Cancers] |
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| Daiichi Sankyo Company, Ltd. announced that the first patient has been dosed in a phase II study evaluating patritumab deruxtecan, a HER3 directed DXd antibody drug conjugat, in patients with advanced or metastatic colorectal cancer who are resistant, refractory, or intolerant to at least two prior lines of systemic therapy.
[Daiichi Sankyo Company, Ltd.] |
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| | Chr. Hansen A/S – Hørsholm, Denmark |
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| | Baylor College of Medicine – Houston, Texas, United States |
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| | The University of Arizona – Tucson, Arizona, United States |
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| | City of Hope – Monrovia, California, United States |
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| | Emory University – Atlanta, Georgia, United States |
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