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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GINS2 Promotes EMT in Pancreatic Cancer via Specifically Stimulating ERK/MAPK Signaling

Investigators found that overexpression of Go-Ichi-Ni-San 2 (GINS2) contributed to advanced clinical stage of pancreatic cancer patient and promoted epithelial–mesenchymal-transition in vitro and in vivo via specifically activating ERK/MAPK signal pathway.
[Cancer Gene Therapy]
Huang, L., Chen, S., Fan, H., Ji, D., Chen, C., & Sheng, W. (2020). GINS2 promotes EMT in pancreatic cancer via specifically stimulating ERK/MAPK signaling. Cancer Gene Therapy, 1–11. https://doi.org/10.1038/s41417-020-0206-7 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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Mucins in Pancreatic Cancer: A Well‐Established but Promising Family for Diagnosis, Prognosis and Therapy

The authors discuss the important roles of mucins that lead to the lethality of pancreatic adenocarcinoma, particularly MUC1, MUC4, MUC5AC and MUC16 in disease progression, and present a comprehensive analysis of the clinical application of mucins and their promising roles in cancer treatment.
[Journal of Cellular and Molecular Medicine]
Mucins in pancreatic cancer: A well‐established but promising family for diagnosis, prognosis and therapy - Wang - - Journal of Cellular and Molecular Medicine - Wiley Online Library. (n.d.). Retrieved August 4, 2020, from https://onlinelibrary.wiley.com/doi/full/10.1111/jcmm.15684 Cite
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TYME Announces Orphan Drug Designation for SM-88 as Potential Treatment for Patients with Pancreatic Cancer

Tyme Technologies, Inc. announced that the FDA has granted the company Orphan Drug Designation for its lead pipeline candidate, SM-88, as a potential treatment for patients with pancreatic cancer.
[TYME Inc.]
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National Institutes of Health (NIH) Awards Research Grant of $2.59 Million to University of Pittsburgh for Diabetes Gene Therapy Technology Licensed by Genprex

Genprex, Inc. announced that Dr. George K. Gittes, MD of the University of Pittsburgh, was awarded a grant of $2.59 million from the NIH National Institute of Diabetes and Digestive and Kidney Diseases.
[Genprex Inc.]
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Twitter Account of Embattled #MeTooSTEM Founder Suspended

Twitter has suspended the account of MeTooSTEM founder BethAnn McLaughlin after allegations emerged that the former Vanderbilt University neuroscientist fabricated the Twitter account of an apparently nonexistent female Native American anthropologist at Arizona State University who had claimed to be an anonymous victim of sexual harassment by a Harvard professor.
[ScienceInsider]
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Hotspot Mutant p53-R273H Inhibits KLF6 Expression to Promote Cell Migration and Tumor Metastasis

Scientists revealed an important role for EGFR–AKT–FOXO1–KLF6–E-cadherin axis in mutant p53-induced cell migration and tumor metastasis.
[Cell Death & Disease]
Sun, S., Chen, H., Sun, L., Wang, M., Wu, X., & Xiao, Z.-X. J. (2020). Hotspot mutant p53-R273H inhibits KLF6 expression to promote cell migration and tumor metastasis. Cell Death & Disease, 11(7), 1–9. https://doi.org/10.1038/s41419-020-02814-1 Cite
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