| Vol. 6.42 – 30 October, 2020 |
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| Scientists showed that nifedipine, a calcium channel blocker, inhibited calcium influx to impair nuclear factor of activated T cell 2 dephosphorylation, activation, and nuclear translocation, thus preventing transcriptional activation of downstream signaling molecules to suppress colorectal cancer proliferation and metastasis. [Cell Reports] |
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| PUBLICATIONSRanked by the impact factor of the journal |
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| Over 600 guide RNAs including the ones targeting LGALS2 were highly enriched in survived cells after sublethal H2O2 challenge. DSS-induced colitis model and AOM/dextran sodium sulfate(DSS)-induced colorectal cancer model showed Galectin2(Gal2) loss ameliorated experimental acute colitis but promoted tumor growth. Mechanically, Gal2 deficiency activated STAT3, promoting colorectal tumor cell growth. Overall, the researchers supported a suppressive role of Gal2 in the colorectal tumor development. [Oncogene] |
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| Cancer stem cells were isolated from human colon cancer cell lines, where the stemness of the cells was evaluated by cell viability, colony-forming, spheroid-forming, invasion, migration, and apoptosis assays. [Journal of Experimental & Clinical Cancer Research] |
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| Intestine-specific N-myc downstream-regulated gene 2 (Ndrg2) deficiency mice were subjected to DSS- or TNBS-induced colitis, and AOM-DSS-induced colitis-associated tumor. HT29 cells, Caco2 cells, primary intestinal epithelial cells from Ndrg2ΔIEC mice, mouse embryo fibroblasts from systemic Ndrg2 knockout mice, HEK293 cells and human UC and DC specimens were used to investigate NDRG2 function in colitis and colitis-associated tumor. [EBioMedicine] |
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| Investigators showed that the interaction between LUCAT1 and Nucleolin (NCL) interferes NCL-mediated inhibition of MYC and promote the expression of MYC. Cells lacking LUCAT1 show a decreased MYC expression, and NCL knockdown rescue LUCAT1 depletion-induced inhibition of colorectal cancer cell proliferation and MYC expression. [Cell Death & Disease] |
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| Gene set enrichment analysis and additional assays confirmed that ETV5 could promote angiogenesis by inducing the secretion of another tumor angiogenesis factor (CCL2) in CRC cells to facilitate Bevacizumab resistance. [Cell Death & Disease] |
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| Using human biopsies, scientists found angulin-1 was downregulated in active Crohn’s disease compared with both controls and Crohn’s disease in remission. In T84 and Caco-2 monolayers, leptin, a cytokine secreted by fat tissue and affected in Crohn’s disease, decreased angulin-1 expression. This effect was completely blocked by STAT3 inhibitors, Stattic and WP1066, but only partially by JAK2 inhibitor AG490. [International Journal of Molecular Sciences] |
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| Researchers established CPT11-resistant variants of three human colon cancer cell lines, and found that gain of the resistance elicited an up-regulation of aldo-keto reductase 1C3 in the cells. [Chemico-Biological Interactions] |
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| Scientists utilized mice and small intestinal organoid models to clarify the role of L-arginine on epithelial differentiation of intestinal stem cells (ISCs). They showed that L-arginine increased expansion of ISCs in mice. [Communications Biology] |
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| The authors discuss recent breakthroughs in the field and highlight different models for functional ex vivo organoid or enteroid derived culture systems. [Current Opinion in Microbiology] |
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| Daiichi Sankyo Company, Limited and AstraZeneca’s ENHERTU has received acceptance for its supplemental Biologics License Application and has also been granted Priority Review in the US for the treatment of patients with HER2 positive metastatic gastric or gastroesophageal junction adenocarcinoma. [Daiichi Sankyo Company, Ltd] |
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| January 25 – January 28, 2021 Virtual |
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| Dalhousie University – Halifax, Nova Scotia, Canada |
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| The University of Utah – Salt Lake City, Utah, United States |
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| University of Minnesota – Minneapolis, Minnesota, United States |
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| Lerner Research Institute – Cleveland, Ohio, United States |
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| Moffitt Cancer Center – Tampa, Florida, United States |
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