NADK Is Activated by Oncogenic Signaling to Sustain Pancreatic Ductal Adenocarcinoma

Scientists showed that oncogenic KRAS promoted protein kinase C-mediated NAD+ kinase (NADK) phosphorylation, leading to its hyperactivation, thus sustaining both NADP+ and NADPH levels in pancreatic ductal adenocarcinoma cells.
[Cell Reports]
Schild, T., McReynolds, M. R., Shea, C., Low, V., Schaffer, B. E., Asara, J. M., Piskounova, E., Dephoure, N., Rabinowitz, J. D., Gomes, A. P., & Blenis, J. (2021). NADK is activated by oncogenic signaling to sustain pancreatic ductal adenocarcinoma. Cell Reports, 35(11). https://doi.org/10.1016/j.celrep.2021.109238 Cite
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Peripherally Active Dextromethorphan Derivatives Lower Blood Glucose Levels by Targeting Pancreatic Islets

Investigators showed that basic nitrogen-containing residues blocked central adverse events of Dextromethorphan without reducing its anti-diabetic effects, including the protection of human pancreatic islets from cell death.
[Cell Chemical Biology]
Scholz, O., Otter, S., Welters, A., Wörmeyer, L., Dolenšek, J., Klemen, M. S., Pohorec, V., Eberhard, D., Mrugala, J., Hamacher, A., Koch, A., Sanz, M., Hoffmann, T., Hogeback, J., Herebian, D., Klöcker, N., Piechot, A., Mayatepek, E., Meissner, T., … Lammert, E. (2021). Peripherally active dextromethorphan derivatives lower blood glucose levels by targeting pancreatic islets. Cell Chemical Biology, 0(0). https://doi.org/10.1016/j.chembiol.2021.05.011 Cite
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Necroptosis Protects against Exacerbation of Acute Pancreatitis

Researchers found that Ripk3−/− mice had significantly more severe pancreatic edema and inflammation associated with macrophage and neutrophil infiltration than control mice.
[Cell Death & Disease]
Boonchan, M., Arimochi, H., Otsuka, K., Kobayashi, T., Uehara, H., Jaroonwitchawan, T., Sasaki, Y., Tsukumo, S., & Yasutomo, K. (2021). Necroptosis protects against exacerbation of acute pancreatitis. Cell Death & Disease, 12(6), 1–13. https://doi.org/10.1038/s41419-021-03847-w Cite
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SETD4-Expressing Cells Contribute to Pancreatic Development and Response to Cerulein Induced Pancreatitis Injury

Scientists provide a new cellular narrative for pancreatic development, homeostasis and response to injury via a small SETD4+ cell population.
[Scientific Reports]
Tian, J.-Z., Xing, S., Feng, J.-Y., Yang, S.-H., Ding, Y.-F., Huang, X.-T., Yang, J.-S., & Yang, W.-J. (2021). SETD4-expressing cells contribute to pancreatic development and response to cerulein induced pancreatitis injury. Scientific Reports, 11(1), 12614. https://doi.org/10.1038/s41598-021-92075-5 Cite
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CF33-hNIS-antiPDL1 Virus Primes Pancreatic Ductal Adenocarcinoma for Enhanced Anti-PD-L1 Therapy

Oncolytic viral chimera, CF33-hNIS-antiPDL1 genetically modified to express anti-human PD-L1 antibody and CF33-hNIS-Δ without the anti-PD-L1 gene, were used to investigate the immunogenic effects of oncolytic virus and virus-delivered anti-PD-L1 in pancreatic ductal adenocarcinoma in vitro.
[Cancer Gene Therapy]
Zhang, Z., Yang, A., Chaurasiya, S., Park, A. K., Lu, J., Kim, S.-I., Warner, S. G., Yuan, Y.-C., Liu, Z., Han, H., Von Hoff, D., Fong, Y., & Woo, Y. (2021). CF33-hNIS-antiPDL1 virus primes pancreatic ductal adenocarcinoma for enhanced anti-PD-L1 therapy. Cancer Gene Therapy, 1–12. https://doi.org/10.1038/s41417-021-00350-4 Cite
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Induction of Cell Death in Pancreatic Tumors by Zinc and Its Fluorescence Chelator TSQ

Scientists found that EPCAM + tumors developed in the mouse pancreas store zinc that is detectable by fluorescence-activated cell sorting using N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide (TSQ), a fluorescence chelator. EPCAM + TSQ + tumor cells isolated from the mouse pancreas formed organoids in matrigel.
[Biological Trace Element Research]
Asahina, K. (2021). Induction of Cell Death in Pancreatic Tumors by Zinc and Its Fluorescence Chelator TSQ. Biological Trace Element Research. https://doi.org/10.1007/s12011-021-02770-7 Cite
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Combinations of Phytochemicals More Efficiently than Single Components Activate Nrf2 and Induce the Expression of Antioxidant Enzymes in Pancreatic Cancer Cells

Human pancreatic cancer cells MIA-Pa-Ca-2 were treated with the phytochemicals alone or their equimolar mixture for 24 h and activation of Nrf2 and expression of its target genes were evaluated.
[Nutrition and Cancer-An International Journal]
Cykowiak, M., Krajka-Kuźniak, V., & Baer-Dubowska, W. (2021). Combinations of Phytochemicals More Efficiently than Single Components Activate Nrf2 and Induce the Expression of Antioxidant Enzymes in Pancreatic Cancer Cells. Nutrition and Cancer, 0(0), 1–16. https://doi.org/10.1080/01635581.2021.1933097 Cite
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Induction of Cell Death in Pancreatic Tumors by Zinc and Its Florescence Chelator TSQ

Upon treatment with N,N,N′,N′-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine, a zinc chelator, organoids degenerated and its negative effect was rescued by co-treatment with zinc, indicating that zinc is necessary for the growth and survival of tumor organoids.
[Biological Trace Element Research]
Asahina, K. (2021). Induction of Cell Death in Pancreatic Tumors by Zinc and Its Fluorescence Chelator TSQ. Biological Trace Element Research. https://doi.org/10.1007/s12011-021-02770-7 Cite
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Chemical Combinations Potentiate Human Pluripotent Stem Cell-Derived 3D Pancreatic Progenitor Clusters toward Functional β Cells

To efficiently cluster hPSC-derived pancreatic progenitors into 3D structures, scientists discovered 10 chemicals that not only retained the pancreatic progenitors in 3D clusters but also enhanced their potentiality towards NKX6.1+/INS+β cells.
[Nature Communications]
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NR4A1 Enhances MKP7 Expression to Diminish JNK Activation Induced by ROS or ER-Stress in Pancreatic β Cells for Surviving

To search other possible mechanisms, scientists found the mRNA level and protein level of MKP7 (a phosphatase for phospho-JNK) were dramatically reduced in pancreatic β cells in the islets from NR4A1 knockout mice compared with that from wild type mice.
[Cell Death & Disease]
Pu, Z., Yu, T., Liu, D., Jin, C., Sadiq, E., Qiao, X., Li, X., Chen, Y., Zhang, J., Tian, M., Li, S., Zhao, R., & Wang, X. (2021). NR4A1 enhances MKP7 expression to diminish JNK activation induced by ROS or ER-stress in pancreatic β cells for surviving. Cell Death Discovery, 7(1), 1–13. https://doi.org/10.1038/s41420-021-00521-0 Cite
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Abnormal Expression of microRNA-296-3p in Type 2 Diabetes Patients and its Role in Pancreatic β-Cells Function by Targeting Tensin Homolog Deleted on Chromosome Ten

Min6 cells were induced by 5 mg/dl UA and the cell proliferation, apoptosis, and insulin release were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry and glucose-stimulated insulin secretion, respectively.
[Biochemical Genetics]
Cheng, M., Guo, Y., Zhong, W., Chen, X., & Guo, G. (2021). Abnormal Expression of microRNA-296-3p in Type 2 Diabetes Patients and its Role in Pancreatic β-Cells Function by Targeting Tensin Homolog Deleted on Chromosome Ten. Biochemical Genetics. https://doi.org/10.1007/s10528-021-10083-6 Cite
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