Protease-Activated Receptor-1 Drives and Maintains Ductal Cell-Fates in the Premalignant Pancreas and Ductal Adenocarcinoma

Scientists found that genetic deficiency for protease‐activated receptor 1(PAR1) increases acinar gene expression programs in the healthy pancreas and that PAR1 deficiency limits ductal transdifferentiation in experimental systems for acinar‐to‐ductal metaplasia.
[Molecular Oncology]
Tekin, C., Scicluna, B. P., Lodestijn, S. C., Shi, K., Bijlsma, M. F., & Spek, C. A. (n.d.). Protease-activated receptor-1 drives and maintains ductal cell-fates in the premalignant pancreas and ductal adenocarcinoma. Molecular Oncology, n/a(n/a). https://doi.org/https://doi.org/10.1002/1878-0261.12971 Cite
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MECOM Permits Pancreatic Acinar Cell Dedifferentiation Avoiding Cell Death under Stress Conditions

The authors applied a non-genetic lineage tracing method of human pancreatic exocrine acinar and duct cells that allowed cell-type-specific gene expression profiling by RNA sequencing.
[Cell Death & Differentiation]
Backx, E., Wauters, E., Baldan, J., Van Bulck, M., Michiels, E., Heremans, Y., De Paep, D. L., Kurokawa, M., Goyama, S., Bouwens, L., Jacquemin, P., Houbracken, I., & Rooman, I. (2021). MECOM permits pancreatic acinar cell dedifferentiation avoiding cell death under stress conditions. Cell Death & Differentiation, 1–15. https://doi.org/10.1038/s41418-021-00771-6 Cite
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Dynamic Regulation of Expression of KRAS and Its Effectors Determines the Ability to Initiate Tumorigenesis in Pancreatic Acinar Cells

The authors revealed that control of the expression of KRAS and its effectors regulated the sensitivity of acinar cells to transformation by oncogenic Kras mutations.
[Cancer Research]
Assi, M., Achouri, Y., Loriot, A., Dauguet, N., Dahou, H., Baldan, J., Libert, M., Fain, J. S., Guerra, C., Bouwens, L., Barbacid, M., Lemaigre, F. P., & Jacquemin, P. (2021). Dynamic regulation of expression of KRAS and its effectors determines the ability to initiate tumorigenesis in pancreatic acinar cells. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-20-2976 Cite
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Pancreatic Glycoprotein 2 Is a First Line of Defense for Mucosal Protection in Intestinal Inflammation

Scientists showed that secretion of luminal glycoprotein 2 from pancreatic acinar cells was induced in a TNF–dependent manner in mice with chemically induced colitis.
[Nature Communications]
Kurashima, Y., Kigoshi, T., Murasaki, S., Arai, F., Shimada, K., Seki, N., Kim, Y.-G., Hase, K., Ohno, H., Kawano, K., Ashida, H., Suzuki, T., Morimoto, M., Saito, Y., Sasou, A., Goda, Y., Yuki, Y., Inagaki, Y., Iijima, H., … Kiyono, H. (2021). Pancreatic glycoprotein 2 is a first line of defense for mucosal protection in intestinal inflammation. Nature Communications, 12(1), 1067. https://doi.org/10.1038/s41467-021-21277-2 Cite
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The EGFR-HSF1 Axis Accelerates the Tumorigenesis of Pancreatic Cancer

Investigators clarified the mechanisms on early activation of heat shock factor 1 (HSF1) and its role in the pancreatic cancer tumorigenesis.
[Journal of Experimental & Clinical Cancer Research]
Qian, W., Chen, K., Qin, T., Xiao, Y., Li, J., Yue, Y., Zhou, C., Ma, J., Duan, W., Lei, J., Han, L., Li, L., Shen, X., Wu, Z., Ma, Q., & Wang, Z. (2021). The EGFR-HSF1 axis accelerates the tumorigenesis of pancreatic cancer. Journal of Experimental & Clinical Cancer Research, 40(1), 25. https://doi.org/10.1186/s13046-020-01823-4 Cite
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Concerted Cell and In Vivo Screen for Pancreatic Ductal Adenocarcinoma (PDA) Chemotherapeutics

Cultured primary PDA cells expressed Rgs16::GFP in response to cytotoxic drugs. A histone deacetylase inhibitor, TSA, stimulated Rgs16::GFP expression in PDA primary cells, potentiated gemcitabine and JQ1 cytotoxicity in cell culture, and Gem + TSA + JQ1 inhibited tumor initiation and progression in vivo.
[Scientific Reports]
Layeghi-Ghalehsoukhteh, S., Pal Choudhuri, S., Ocal, O., Zolghadri, Y., Pashkov, V., Niederstrasser, H., Posner, B. A., Kantheti, H. S., Azevedo-Pouly, A. C., Huang, H., Girard, L., MacDonald, R. J., Brekken, R. A., & Wilkie, T. M. (2020). Concerted cell and in vivo screen for pancreatic ductal adenocarcinoma (PDA) chemotherapeutics. Scientific Reports, 10(1), 20662. https://doi.org/10.1038/s41598-020-77373-8 Cite
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EMC6 Regulates Acinar Apoptosis via APAF1 in Acute and Chronic Pancreatitis

Potential regulatory proteins in pancreatitis were identified by proteomic screen using pancreatic tissues of PRSS1Tg AP mice. Adenoviral shRNA-mediated knockdown of identified proteins, followed by functional assays was performed to validate their roles.
[Cell Death & Disease]
Tan, J., Cao, R., Zhou, L., Zhou, Z., Chen, H., Xu, J., Chen, X., Jin, Y., Lin, J., Qi, Z., Zeng, J., Li, S., Luo, M., Hu, G., Jin, J., & Zhang, G. (2020). EMC6 regulates acinar apoptosis via APAF1 in acute and chronic pancreatitis. Cell Death & Disease, 11(11), 1–13. https://doi.org/10.1038/s41419-020-03177-3 Cite
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Pancreas-Specific Deletion of Protein Kinase D Attenuates Inflammation, Necrosis, and Severity of Acute Pancreatitis

Investigators generated a mouse model with pancreas-specific deletion of PKD3, the predominant PKD isoform in mouse pancreatic acinar cells, by crossing Pkd3flox/flox mice with Pdx1-Cre transgenic mice which express Cre recombinase under the control of the mouse Pdx1 promoter.
[Biochimica Et Biophysica Acta-Molecular Basis of Disease]
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Single-Cell Transcriptomes of Pancreatic Preinvasive Lesions and Cancer Reveal Acinar Metaplastic Cells’ Heterogeneity

Using a reporter gene, scientists identified metaplastic cells that originated from acinar cells and expressed two transcription factors, Onecut2 and Foxq1. Further analyses of metaplastic acinar cell heterogeneity defined six acinar metaplastic cell types and states, including stomach-specific cell types.
[Nature Communications]

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The Gustatory Sensory G-Protein GNAT3 Suppresses Pancreatic Cancer Progression in Mice

Compromised gustatory sensing, achieved by Gnat3 ablation, enhanced the CXCL1/2 – CXCR2 axis to alter the myeloid-derived suppressor cell population and promoted the progression of metastatic pancreatic ductal adenocarcinoma.
[Cellular and Molecular Gastroenterology and Hepatology]

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Lumenal Galectin-9-Lamp2 Interaction Regulates Lysosome and Autophagy to Prevent Pathogenesis in the Intestine and Pancreas

Investigators showed in gut epithelial cells, that galectin-9 was enriched in lysosomes and predominantly bound to lysosome-associated membrane protein 2 (Lamp2) in a Asn(N)-glycan dependent manner.
[Nature Communications]
Sudhakar, J. N., Lu, H.-H., Chiang, H.-Y., Suen, C.-S., Hwang, M.-J., Wu, S.-Y., Shen, C.-N., Chang, Y.-M., Li, F.-A., Liu, F.-T., & Shui, J.-W. (2020). Lumenal Galectin-9-Lamp2 interaction regulates lysosome and autophagy to prevent pathogenesis in the intestine and pancreas. Nature Communications, 11(1), 4286. https://doi.org/10.1038/s41467-020-18102-7 Cite
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