scholarly journals S100A6 binds to annexin 2 in pancreatic cancer cells and promotes pancreatic cancer cell motility

2009 ◽  
Vol 101 (7) ◽  
pp. 1145-1154 ◽  
Author(s):  
T Nedjadi ◽  
N Kitteringham ◽  
F Campbell ◽  
R E Jenkins ◽  
B K Park ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Motility ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Motility ◽  
Pancreatic Cancer Cells ◽  
Annexin 2

S2006 The Role of TRPC and Na+/CA2+ Exchanger in Mediating TGFβ-Induced Pancreatic Cancer Cell Motility

2009 ◽  
Vol 136 (5) ◽  
pp. A-311
Author(s):  
Jimmy Chow ◽  
Ki-Nam Shim ◽  
Tiffany A. Ornelas ◽  
Jonathan K. Lee ◽  
John M. Carethers ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Motility ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Motility

scholarly journals Blocking IL-6/GP130 Signaling Inhibits Cell Viability/Proliferation, Glycolysis, and Colony Forming Activity in Human Pancreatic Cancer Cells

2019 ◽  
Vol 19 (5) ◽  
pp. 417-427 ◽  
Author(s):  
Xiang Chen ◽  
Jilai Tian ◽  
Gloria H. Su ◽  
Jiayuh Lin
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Human Pancreatic Cancer ◽  
Multiple Cancer ◽  
Pancreatic Cancer Cells ◽  
Stat3 Phosphorylation

Background:Elevated production of the pro-inflammatory cytokine interleukin-6 (IL-6) and dysfunction of IL-6 signaling promotes tumorigenesis and are associated with poor survival outcomes in multiple cancer types. Recent studies showed that the IL-6/GP130/STAT3 signaling pathway plays a pivotal role in pancreatic cancer development and maintenance.Objective:We aim to develop effective treatments through inhibition of IL-6/GP130 signaling in pancreatic cancer.Methods:The effects on cell viability and cell proliferation were measured by MTT and BrdU assays, respectively. The effects on glycolysis was determined by cell-based assays to measure lactate levels. Protein expression changes were evaluated by western blotting and immunoprecipitation. siRNA transfection was used to knock down estrogen receptor α gene expression. Colony forming ability was determined by colony forming cell assay.Results:We demonstrated that IL-6 can induce pancreatic cancer cell viability/proliferation and glycolysis. We also showed that a repurposing FDA-approved drug bazedoxifene could inhibit the IL-6/IL-6R/GP130 complexes. Bazedoxifene also inhibited JAK1 binding to IL-6/IL-6R/GP130 complexes and STAT3 phosphorylation. In addition, bazedoxifene impeded IL-6 mediated cell viability/ proliferation and glycolysis in pancreatic cancer cells. Consistently, other IL-6/GP130 inhibitors SC144 and evista showed similar inhibition of IL-6 stimulated cell viability, cell proliferation and glycolysis. Furthermore, all three IL-6/GP130 inhibitors reduced the colony forming ability in pancreatic cancer cells.Conclusion:Our findings demonstrated that IL-6 stimulates pancreatic cancer cell proliferation, survival and glycolysis, and supported persistent IL-6 signaling is a viable therapeutic target for pancreatic cancer using IL-6/GP130 inhibitors.

Identification and characterization of CCK-B/gastrin receptors in human pancreatic cancer cell lines

1994 ◽  
Vol 266 (1) ◽  
pp. R277-R283 ◽  
Author(s):  
J. P. Smith ◽  
G. Liu ◽  
V. Soundararajan ◽  
P. J. McLaughlin ◽  
I. S. Zagon
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Human Pancreatic Cancer ◽  
Human Pancreatic Cancer Cell ◽  
Pancreatic Cancer Cells

The gastrointestinal peptide cholecystokinin (CCK) is known to stimulate growth of human pancreatic cancer in a receptor-mediated fashion. The purpose of this study was to characterize the receptor responsible for the trophic effects of CCK in cancer cells. With the use of homogenates of PANC-1 human pancreatic cancer cells grown in vitro, the binding characteristics and optimal conditions of radiolabeled selective CCK-receptor antagonists ([3H]L-365,260 and [3H]L-364,718) were examined. Specific and saturable binding was detected with [3H]L-365,260, and Scatchard analysis revealed that the data were consistent for a single site of binding with a binding affinity of 4.3 +/- 0.6 nM and a binding capacity (Bmax) of 283 +/- 68 fmol/mg protein in log phase cells. Binding was dependent on protein concentration, time, temperature, and pH and was sensitive to Na+, K+, Mg2+, and ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. In contrast to log phase cells, Bmax decreased by 80 and 92% in confluent and postconfluent cultures, respectively. Subcellular fractionation studies revealed that binding was in the membrane fraction. Competition experiments indicated that L-365,260 and gastrin were more effective at displacing the radiolabeled L-365,260 than CCK. No binding was detected with the CCK-A antagonist [3H]L-364,718. Assays performed with [3H]L-365,260 on five additional human pancreatic cancer cell lines in vitro and tumor tissue from xenografts in nude mice also revealed specific and saturable binding. These results provide the first identification of a CCK-B/gastrin receptor in human pancreatic cancer cells and tumors and explain the effects of CCK on the growth of this malignancy.

Pancreatic Cancer Cells Invasiveness is Mainly Affected by Interleukin-1β not by Transforming Growth Factor-β1

2005 ◽  
Vol 20 (4) ◽  
pp. 235-241 ◽  
Author(s):  
E. Greco ◽  
D. Basso ◽  
P. Fogar ◽  
S. Mazza ◽  
F. Navaglia ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Extracellular Matrix ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Matrigel Invasion ◽  
Matrix Adhesion ◽  
Pancreatic Cancer Cells ◽  
Tgf Β1

Background We investigated in vitro whether IL-1β and TGF-β1 affect pancreatic cancer cell growth, adhesion to the extracellular matrix and Matrigel invasion. Materials and methods Adhesion to fibronectin, laminin and type I collagen, and Matrigel invasion after stimulation with saline, IL-1β and TGF-β1 were evaluated using three primary and three metastatic pancreatic cancer cell lines. Results Extracellular matrix adhesion of control cells varied independently of the metastatic characteristics of the studied cell lines, whereas Matrigel invasion of control cells was partly correlated with the in vivo metastatic potential. IL-1β did not influence extracellular matrix adhesion, whereas it significantly enhanced the invasiveness of three of the six cell lines. TGF-β1 affected the adhesion of one cell line, and exerted contrasting effects on Matrigel invasion of different cell lines. Conclusions IL-1β enhances the invasive capacity of pancreatic cancer cells, whereas TGF-β1 has paradoxical effects on pancreatic cancer cells; this makes it difficult to interfere with TGF-β1 signaling in pancreatic cancer treatment.

Inhibition of peroxisome proliferator-activated receptor γ activity suppresses pancreatic cancer cell motility

2008 ◽  
Vol 99 (10) ◽  
pp. 1892-1900 ◽  
Author(s):  
Atsushi Nakajima ◽  
Ayako Tomimoto ◽  
Koji Fujita ◽  
Michiko Sugiyama ◽  
Hirokazu Takahashi ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Motility ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cancer Cell Motility

scholarly journals Propofol Mediates Pancreatic Cancer Cell Activity Through the Repression of ADAM8 via SP1

2021 ◽  
Author(s):  
Yutong Gao ◽  
Yu Zhou ◽  
Chunlin Wang ◽  
Klarke Sample ◽  
Xiangdi Yu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cell Activity ◽  
Pancreatic Cancer Cell Line ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Physical Interaction ◽  
Pancreatic Cancer Cells

Abstract Background Propofol is a commonly used anesthetic with controversial effects on cancer cells. A growing number of studies have demonstrated that low concentrations of propofol are associated with tumor suppression and when used as an intravenous anesthesia improved recurrence-free survival rates for many cancers, but deeper insights into its underlying mechanism are needed. Methods The study detailed herein focuses upon the effect of propofol on pancreatic cancer cells and the mechanism by which propofol reduces ADAM8 expression. The ability of propofol to impact the proliferation, migration and cell cycle of a pancreatic cancer cell line was assessed in vitro. This was mechanistically explored following the identification of SP1 binding sites within ADAM8, which enabled the regulatory effects of SP1 on ADAM8 following propofol treatment to be further explored. Results This study was able to show that propofol significantly inhibited the proliferation, migration and invasion of pancreatic cancer cells and decreased the percentage of cells in S-phase. Propofol treatment was also shown to repress ADAM8 and SP1 expression, but was unable to affect ADAM8 expression following knockdown of SP1. Moreover, a direct physical interaction between SP1 and ADAM8 was verified using Co-immunoprecipitation and dual-luciferase reporter assays. Conclusion These results suggest that propofol represses pathological biological behaviors associated with pancreatic cancer cells through the suppression of SP1, which in turn results in lower ADAM8 mRNA expression and protein levels.

scholarly journals Fusobacterium nucleatum infection induces pancreatic cancer cell proliferation and migration through regulation of host cytokine signaling

2021 ◽  
Author(s):  
Barath Udayasuryan ◽  
Tam T.D. Nguyen ◽  
Ariana Umana ◽  
LaDeidra Monet Roberts ◽  
Raffae A Ahmad ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Pancreatic Tumor ◽  
Pancreatic Cancer Cell ◽  
Fusobacterium Nucleatum ◽  
Cellular Migration ◽  
Gm Csf ◽  
Pancreatic Cancer Cells

Pancreatic ductal adenocarcinoma (PDAC) harbors a complex tumor microbiome that has been implicated in cancer progression and resistance to chemotherapy. Recent clinical investigations uncovered a correlation between high loads of intratumor Fusobacterium nucleatum and decreased patient survival. Here we show that pancreatic cancer cell lines harboring intracellular F. nucleatum secrete elevated levels of cancer-associated cytokines including IL-8, CXCL1, GM-CSF, and MIP-3α. We report that GM-CSF directly increases the proliferation of pancreatic cancer cells, and contributes to increased cellular migration, notably in the absence of immune cell participation. This study is the first to investigate the direct impact of F. nucleatum infection on pancreatic cancer cells. Our results suggest that F. nucleatum within the pancreatic tumor microenvironment elicits infection-specific cytokine secretion that directly contributes adversely to cancer progression and warrants further research into therapeutic manipulation of the pancreatic tumor microbiome.

scholarly journals 727 – Wnt11 Promotes Pancreatic Cancer Cell Motility and Invasion

2019 ◽  
Vol 156 (6) ◽  
pp. S-1404
Author(s):  
Tara Hughes ◽  
Xinqun Li ◽  
Bingbing Dai ◽  
Christian Siangco ◽  
Kaberi Das ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Motility ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Motility

Hyaluronan stimulates pancreatic cancer cell motility

Pancreatology ◽  
2016 ◽  
Vol 16 (4) ◽  
pp. S69 ◽  
Author(s):  
Xiao-Bo Cheng ◽  
Shiro Kohi ◽  
Atsuhiro Koga ◽  
Keiji Hirata ◽  
Norihiro Sato
Keyword(s):  
Pancreatic Cancer ◽  
Cell Motility ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Motility

221 TGFβ Destabilizes PTEN via Dephosphorylation to Promote Pancreatic Cancer Cell Motility

2010 ◽  
Vol 138 (5) ◽  
pp. S-42
Author(s):  
Jimmy Y. Chow ◽  
Flang Nguyen ◽  
Mei Huang ◽  
John M. Carethers
Keyword(s):  
Pancreatic Cancer ◽  
Cell Motility ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Motility
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