Lentiviral Gene Therapy Vectors Encoding VIP Suppressed Diabetes-Related Inflammation and Augmented Pancreatic Beta-Cell Proliferation

The authors suggested the observed therapeutic effect of lentiviral vector carrying vasoactive intestinal peptide(VIP) gene was due to the repression of diabetes-induced inflammation, its insulinotropic properties, and VIP-induced beta-cell proliferation.
[Gene Therapy]
Erendor, F., Sahin, E. O., Sanlioglu, A. D., Balci, M. K., Griffith, T. S., & Sanlioglu, S. (2020). Lentiviral gene therapy vectors encoding VIP suppressed diabetes-related inflammation and augmented pancreatic beta-cell proliferation. Gene Therapy, 1–12. https://doi.org/10.1038/s41434-020-0183-3 Cite
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Lactate Activation of α-Cell KATP Channels Inhibits Glucagon Secretion by Hyperpolarizing the Membrane Potential and Reducing Ca2+ Entry

Mouse and human islets were used in combination with confocal microscopy, electrophysiology, GCG immunoassays, and fluorescent thallium flux assays to assess α-cell Ca2+ handling, Vm, KATP currents, and GCG secretion.
[Molecular Metabolism]
Zaborska, K. E., Dadi, P. K., Dickerson, M. T., Nakhe, A. Y., Thorson, A. S., Schaub, C. M., Graff, S. M., Stanley, J. E., Kondapavuluru, R. S., Denton, J. S., & Jacobson, D. A. (2020). Lactate activation of α-cell KATP channels inhibits glucagon secretion by hyperpolarizing the membrane potential and reducing Ca2+ entry. Molecular Metabolism, 101056. https://doi.org/10.1016/j.molmet.2020.101056 Cite
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TET1 Downregulates Epithelial-Mesenchymal Transition and Chemoresistance in PDAC by Demethylating CHL1 to Inhibit the Hedgehog Signaling Pathway

In vitro and in vivo functional studies performed by silencing or overexpressing TET1 suggested that TET1 was able to suppress epithelial-mesenchymal transition and sensitize pancreatic ductal adenocarcinoma cells to 5FU and gemcitabine. RNA-seq, whole genome bisulfite sequencing and ChIP-seq were used to explore the TET1-associated pathway, and showed that TET1 promoted the transcription of CHL1 by binding and demethylating the CHL1 promoter, which consequently inhibits the Hedgehog pathway.
[Oncogene]
Li, H., Jiang, W., Liu, X.-N., Yuan, L.-Y., Li, T.-J., Li, S., Xu, S.-S., Zhang, W.-H., Gao, H.-L., Han, X., Wang, W.-Q., Wu, C.-T., Yu, X.-J., Xu, H.-X., & Liu, L. (2020). TET1 downregulates epithelial-mesenchymal transition and chemoresistance in PDAC by demethylating CHL1 to inhibit the Hedgehog signaling pathway. Oncogene, 1–14. https://doi.org/10.1038/s41388-020-01407-8 Cite
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Metformin Inhibits Pancreatic Cancer Metastasis Caused by SMAD4 Deficiency and Consequent HNF4G Upregulation

The authors found that metformin suppressed HNF4G activity via AMPK-mediated phosphorylation-coupled ubiquitination degradation and inhibited in vitro invasion and in vivo metastasis of pancreatic ductal adenocarcinoma cells with SMAD4 deficiency.
[Protein & Cell]
Wang, C., Zhang, T., Liao, Q., Dai, M., Guo, J., Yang, X., Tan, W., Lin, D., Wu, C., & Zhao, Y. (2020). Metformin inhibits pancreatic cancer metastasis caused by SMAD4 deficiency and consequent HNF4G upregulation. Protein & Cell. https://doi.org/10.1007/s13238-020-00760-4 Cite
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IL-17F Induces Inflammation, Dysfunction and Cell Death in Mouse Islets

IL-17F possessed similar pathogenic activities to IL-17A in mouse β-cell lines and islets and was likely to be a type 17 associated pathogenic factor in type 1 diabetes.
[Scientific Reports]
Catterall, T., Fynch, S., Kay, T. W. H., Thomas, H. E., & Sutherland, A. P. R. (2020). IL-17F induces inflammation, dysfunction and cell death in mouse islets. Scientific Reports, 10(1), 13077. https://doi.org/10.1038/s41598-020-69805-2 Cite
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Lentiviral Gene Therapy Vectors Encoding VIP Suppressed Diabetes-Related Inflammation and Augmented Pancreatic Beta-Cell Proliferation

The authors suggest the observed therapeutic effect of lentiviral vector carrying VIP gene was due to the repression of diabetes-induced inflammation, its insulinotropic properties, and VIP-induced beta-cell proliferation.
[Gene Therapy]
Erendor, F., Sahin, E. O., Sanlioglu, A. D., Balci, M. K., Griffith, T. S., & Sanlioglu, S. (2020). Lentiviral gene therapy vectors encoding VIP suppressed diabetes-related inflammation and augmented pancreatic beta-cell proliferation. Gene Therapy, 1–12. https://doi.org/10.1038/s41434-020-0183-3 Cite
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DGAT1 Inhibitors Protect Pancreatic β-Cells from Palmitic Acid-Induced Apoptosis

Researchers evaluated the potential beneficial effects of DGAT1 inhibitors on pancreatic β-cells, and further verified their antidiabetic effects in db/db mice.
[Acta Pharmacologica Sinica]
Huang, J., Guo, B., Wang, G., Zeng, L., Hu, Y., Wang, T., & Wang, H. (2020). DGAT1 inhibitors protect pancreatic β-cells from palmitic acid-induced apoptosis. Acta Pharmacologica Sinica, 1–8. https://doi.org/10.1038/s41401-020-0482-7 Cite
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Lentiviral Gene Therapy Vectors Encoding VIP Suppressed Diabetes-Related Inflammation and Augmented Pancreatic Beta-Cell Proliferation

The therapeutic efficacy of LentiVIP was tested in a multiple low-dose STZ-induced animal model of type 1 diabetes. LentiVIP delivery into diabetic animals reduced hyperglycemia, improved glucose tolerance, and prevented weight loss.
[Gene Therapy]
Erendor, F., Sahin, E. O., Sanlioglu, A. D., Balci, M. K., Griffith, T. S., & Sanlioglu, S. (2020). Lentiviral gene therapy vectors encoding VIP suppressed diabetes-related inflammation and augmented pancreatic beta-cell proliferation. Gene Therapy, 1–12. https://doi.org/10.1038/s41434-020-0183-3 Cite
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Identification of an Anti-Diabetic, Orally Available Small Molecule that Regulates TXNIP Expression and Glucagon Action

In rat cells and in mouse and human islets, SRI-37330 inhibited expression and signaling of thioredoxin-interacting protein, previously found to be elevated in diabetes and to have detrimental effects on islet function.
[Cell Metabolism]
Identification of an Anti-diabetic, Orally Available Small Molecule that Regulates TXNIP Expression and Glucagon Action: Cell Metabolism. (n.d.). Retrieved July 28, 2020, from https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30360-0 Cite
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Insulin2Q104del (Kuma) Mutant Mice Develop Diabetes with Dominant Inheritance

Scientists generated a novel Kuma mutant mice with p.Q104del in the Insulin2 gene in a BRJ background that exhibited a severe immune deficiency.
[Scientific Reports]
Sakano, D., Inoue, A., Enomoto, T., Imasaka, M., Okada, S., Yokota, M., Koike, M., Araki, K., & Kume, S. (2020). Insulin2 Q104del (Kuma) mutant mice develop diabetes with dominant inheritance. Scientific Reports, 10(1), 12187. https://doi.org/10.1038/s41598-020-68987-z Cite
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Invasion Inhibition in Pancreatic Cancer using the Oral Iron Chelating Agent Deferasirox

Researchers used pancreatic cancer cell lines (BxPC-3, Panc-1, and HPAF II) to examine the efficacy of iron chelator deferasirox in preventing invasion in vitro, evaluated using scratch assays and Boyden chamber assays.
[BMC Cancer]
Amano, S., Kaino, S., Shinoda, S., Harima, H., Matsumoto, T., Fujisawa, K., Takami, T., Yamamoto, N., Yamasaki, T., & Sakaida, I. (2020). Invasion inhibition in pancreatic cancer using the oral iron chelating agent deferasirox. BMC Cancer, 20(1), 681. https://doi.org/10.1186/s12885-020-07167-8 Cite
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CircRHOT1 Mediated Cell Proliferation, Apoptosis and Invasion of Pancreatic Cancer Cells by Sponging miR-125a-3p

Investigators demonstrated that circRHOT1 was overexpressed in pancreatic cancer tissues and cell lines, and it was found to directly bind to miR‐125a‐3p, acting as an endogenous sponge to inhibit its activity.
[Journal of Cellular and Molecular Medicine]
Ling, S., He, Y., Li, X., Hu, M., Ma, Y., Li, Y., Lu, Z., Shen, S., Kong, B., Zou, X., Jiang, K., & Huang, P. (n.d.). CircRHOT1 mediated cell proliferation, apoptosis and invasion of pancreatic cancer cells by sponging miR-125a-3p. Journal of Cellular and Molecular Medicine, n/a(n/a). https://doi.org/10.1111/jcmm.15572 Cite
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