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Wang, S
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Publications (5 of 5) Show all publications
Stålberg, P., Grimfjärd, P., Santesson, M., Zhou, Y., Lindberg, D., Gobl, A., . . . Skogseid, B. (2004). Transfection of the multiple endocrine neoplastia type 1 gene to a human endocrine pancreatic tumor cell line inhibits cell growth and affects expression of junD, delta-like protein 1/preadipocyte factor-1, proliferating cell nuclear antigen and QM/Jif-1. The journal of clinical endocrinology & metabolism, 5, 2326-2337
Open this publication in new window or tab >>Transfection of the multiple endocrine neoplastia type 1 gene to a human endocrine pancreatic tumor cell line inhibits cell growth and affects expression of junD, delta-like protein 1/preadipocyte factor-1, proliferating cell nuclear antigen and QM/Jif-1
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2004 (English)In: The journal of clinical endocrinology & metabolism, Vol. 5, p. 2326-2337Article in journal (Refereed) Published
Keywords
Aged, Antibody Specificity, Carcinoid Tumor/blood/chemistry, Chromogranins/*blood/chemistry, Endocrine Gland Neoplasms/blood/chemistry, Female, Humans, Male, Middle Aged, Neuroendocrine Tumors/*blood, Pancreatic Neoplasms/blood/chemistry, Peptide Library, Radioimmunoassay/*methods, Research Support; Non-U.S. Gov't
Identifiers
urn:nbn:se:uu:diva-65563 (URN)
Available from: 2005-09-13 Created: 2005-09-13 Last updated: 2011-01-12
Zhou, Y., Wang, S., Yue, B., Gobl, A. & Oberg, K. (2002). Effects of interferon alpha on the expression of p21cip1/waf1 and cellcycle distribution in carcinoid tumors.. Cancer Invest, 20, 348
Open this publication in new window or tab >>Effects of interferon alpha on the expression of p21cip1/waf1 and cellcycle distribution in carcinoid tumors.
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2002 (English)In: Cancer Invest, Vol. 20, p. 348-Article in journal (Refereed) Published
Abstract [en]

Interferon alpha (IFN-alpha) has been shown to produce antitumor effects in 50-80% of carcinoid tumor patients and has demonstrated anti-proliferative effects in carcinoid tumor cells, but the mechanism is not well established. This study presents evidence that in a carcinoid tumor cell line, Bon1, IFN-alpha increases the expression of p21 and promotes nuclear translocation of endogenous p21. Furthermore, immunoprecipitation experiments demonstrated that p21 formed immuno-complexes with Stat1 and Stat2 in the nucleus of cells. Interferon alpha can decrease G1- and G2-phase cells, but increase S-phase population. The p21 mRNA expression is inversely correlated to the G1 population (r = -0.933, P < 0.05) and positively correlated to the S-phase population (r = 0.901, P < 0.05). In addition, IFN-alpha inhibited cyclin dependent kinases (CDK), CDK2-, CDK3-, CDK4-, and cyclin E- but not cyclin A-associated kinase activities. Immunodepletion of p21 resulted in a significant enhancement of CDK3 kinase activity (approximately 1.6-fold increase). These results suggest that the mechanism of antitumor and cell cycle regulation of IFN-alpha in carcinoid tumors may, at least in part, be p21-dependent. Based on these results, we conclude that IFN-alpha exerts antitumor effects by increased p21 expression in neuroendocrine tumors.

Keywords
interferon alpha, gene expression, p21Cip1/Waf1, signal transduction, carcinoid, neuroendocrine tumor, cell cycle, cyclin dependent kinase
Identifiers
urn:nbn:se:uu:diva-65540 (URN)
Available from: 2008-06-15 Created: 2008-06-15 Last updated: 2011-01-13
Stålberg, P., Lopez-Egido, J. R., Wang, S., Gobl, A., Oberg, K. & Skogseid, B. (2001). Differentially expressed cDNAs in PLCbeta3-induced tumor suppression in a human endocrine pancreatic tumor cell line: activation of the human mismatch repair protein 3 gene.. Biochem Biophys Res Commun, 281(1), 227-31
Open this publication in new window or tab >>Differentially expressed cDNAs in PLCbeta3-induced tumor suppression in a human endocrine pancreatic tumor cell line: activation of the human mismatch repair protein 3 gene.
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2001 (English)In: Biochem Biophys Res Commun, ISSN 0006-291X, Vol. 281, no 1, p. 227-31Article in journal (Refereed) Published
Keywords
Animals, Apoptosis Regulatory Proteins, Base Pair Mismatch, Blotting; Northern, Calcium-Binding Proteins/metabolism, Chromogranins/metabolism, DNA Repair, DNA; Complementary/*metabolism, DNA-Binding Proteins/*metabolism, Down-Regulation, Enzyme Activation, Gene Expression Profiling, Humans, Isoenzymes/*metabolism, Mice, Multidrug Resistance-Associated Proteins, Phenotype, Phospholipase C/*metabolism, Plasmids/metabolism, Polymerase Chain Reaction, Protein Isoforms, Proteins/metabolism, RNA-Binding Proteins, Research Support; Non-U.S. Gov't, Reverse Transcriptase Polymerase Chain Reaction, S100 Proteins, Signal Transduction, Transfection, Tumor Cells; Cultured
Identifiers
urn:nbn:se:uu:diva-18658 (URN)11178984 (PubMedID)
Available from: 2007-01-22 Created: 2007-01-22 Last updated: 2017-01-25
Wang, S., Lukinius, A., Zhou, Y., Stålberg, P., Gobl, A., Oberg, K. & Skogseid, B. (2000). Subcellular distribution of phospholipase C isoforms in rodent pancreas and gastric mucosa.. Endocrinology, 141(7), 2589-93
Open this publication in new window or tab >>Subcellular distribution of phospholipase C isoforms in rodent pancreas and gastric mucosa.
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2000 (English)In: Endocrinology, ISSN 0013-7227, Vol. 141, no 7, p. 2589-93Article in journal (Refereed) Published
Keywords
Animals, Gastric Mucosa/*enzymology, Islets of Langerhans/cytology/enzymology, Isoenzymes/*metabolism, Mice, Mice; Inbred C57BL, Pancreas/cytology/*enzymology, Phospholipase C/*metabolism, Rats, Rats; Sprague-Dawley, Research Support; Non-U.S. Gov't, Subcellular Fractions/enzymology, Tissue Distribution
Identifiers
urn:nbn:se:uu:diva-83736 (URN)10875262 (PubMedID)
Available from: 2008-05-16 Created: 2008-05-16 Last updated: 2017-01-25
Wang, S., Lukinius, A., Zhou, Y., Stålberg, P., Gobl, A., Öberg, K. & Skogseid, B. (2000). Subcellular distribution of phospholipase C isoforms in rodent pancreas and gastric mucosa. Endocrinology, 141(7), 2589-2593
Open this publication in new window or tab >>Subcellular distribution of phospholipase C isoforms in rodent pancreas and gastric mucosa
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2000 (English)In: Endocrinology, ISSN 0013-7227, E-ISSN 1945-7170, Vol. 141, no 7, p. 2589-2593Article in journal (Refereed) Published
Abstract [en]

Phosphoinositide-specific phospholipase C (PLC) has been implicated as a participant in cell proliferation as well as enzyme and hormone secretion. Defining the subcellular distribution of PLC isoforms would possibly contribute to further understanding of their function. We investigated the intracellular distribution of four PLCs (β1, β2, β3, and γ1) in mouse pancreatic cells as well as mouse and rat gastric mucosa cells by ultrastructural immunocytochemistry. In pancreatic acinar cells, PLCβ1 and PLCγ1 were demonstrated in the zymogen granules while PLCβ2 was present in the granulae as well as the endoplasmic reticulum (ER), and PLCβ3 was prominent in the ER. In the endocrine pancreas, PLCβ2 immunolabeling was expressed in the secretory granulae of α, β, δ, and pancreatic polypeptide cells. PLCβ3 showed a slight labeling in the nucleus and ER of all four pancreatic endocrine cell types while PLCγ1 was prominent in α cell granulae. In the gastric mucosa cells, PLCβ2 was highly expressed in the heterochromatin areas and in the ER of parietal, chief, mucous, and enterochromaffin-like cells. PLCβ3 were expressed in a manner similar to PLCβ2 in those cells; however, no immunoreaction was seen in the ER of parietal cell. PLCγ1 was demonstrated in the chief cell granulae. One possible, although yet speculative, interpretation of our results is that the studied PLC isoforms may be involved in processing in pancreatic secretory granulae and that nuclear PLCβ2 and PLCβ3 signaling pathways may be operative in the cells of the gastric mucosa.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-51504 (URN)10.1210/en.141.7.2589 (DOI)10875262 (PubMedID)
Available from: 2008-10-17 Created: 2008-10-17 Last updated: 2017-12-04Bibliographically approved
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