scholarly journals The influence of SnoN gene silencing by siRNA on the cell proliferation and apoptosis of human pancreatic cancer cells

2015 ◽  
Vol 10 (1) ◽  
Author(s):  
Chengli Liu ◽  
Hui Zhang ◽  
Xiaoxia Zang ◽  
Cheng Wang ◽  
Yalin Kong ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Gene Silencing ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Proliferation And Apoptosis

scholarly journals The effects of cyclooxygenase-2 gene silencing by siRNA on cell proliferation, cell apoptosis, cell cycle and tumorigenicity of Capan-2 human pancreatic cancer cells

2011 ◽  
Vol 27 (4) ◽  
pp. 1003-1010 ◽  
Author(s):  
YINGQIANG ZHONG ◽  
ZHONGSHENG XIA ◽  
JUAN LIU ◽  
YING LIN ◽  
HUI ZAN
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Gene Silencing ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Cyclooxygenase 2 ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells

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.

scholarly journals Protease-activated receptor 2 agonist increases cell proliferation and invasion of human pancreatic cancer cells

2014 ◽  
Vol 9 (1) ◽  
pp. 239-244 ◽  
Author(s):  
LIQUN XIE ◽  
ZEXING DUAN ◽  
CAIJU LIU ◽  
YANMIN ZHENG ◽  
JING ZHOU
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Protease Activated Receptor 2 ◽  
Proliferation And Invasion

Thymosinα1 stimulates cell proliferation by activating ERK1/2, JNK, and increasing cytokine secretion in human pancreatic cancer cells

2007 ◽  
Vol 248 (1) ◽  
pp. 58-67 ◽  
Author(s):  
Min Li ◽  
Louis W. Feurino ◽  
Fei Li ◽  
Hao Wang ◽  
Qihui Zhai ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cytokine Secretion ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells

Cyclophilin A is overexpressed in human pancreatic cancer cells and stimulates cell proliferation through CD147

Cancer ◽  
2006 ◽  
Vol 106 (10) ◽  
pp. 2284-2294 ◽  
Author(s):  
Min Li ◽  
Qihui Zhai ◽  
Uddalak Bharadwaj ◽  
Hao Wang ◽  
Fei Li ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cyclophilin A ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells

Antifibrotic Agent Pirfenidone Suppresses Proliferation of Human Pancreatic Cancer Cells by Inducing G0/G1 Cell Cycle Arrest

Pharmacology ◽  
2019 ◽  
Vol 103 (5-6) ◽  
pp. 250-256 ◽  
Author(s):  
Eri Usugi ◽  
Kenichiro Ishii ◽  
Yoshifumi Hirokawa ◽  
Kazuki Kanayama ◽  
Chise Matsuda ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Experimental Conditions ◽  
Cycle Arrest ◽  
Pancreatic Cancer Cells ◽  
G1 Cell Cycle Arrest

Background: Pirfenidone (PFD), which is an antifibrotic agent used for treatment of idiopathic pulmonary fibrosis, induces G0/G1 cell cycle arrest in fibroblasts. We hypothesized that PFD-induced G0/G1 cell cycle arrest might be achieved in other types of cells, including cancer cells. Here we investigated the effects of PFD on the proliferation of pancreatic cancer cells (PCCs) in vitro. Method: Human skin fibroblasts ASF-4-1 cells and human prostate stromal cells (PrSC) were used as fibroblasts. PANC-1, MIA PaCa-2, and BxPC-3 cells were used as human PCCs. Cell cycle and apoptosis were analyzed using flow cytometer. Results: First, we confirmed that PFD suppressed cell proliferation of ASF-4-1 cells and PrSC and induced G0/G1 cell cycle arrest. Under these experimental conditions, PFD also suppressed cell proliferation and induced G0/G1 cell cycle arrest in all PCCs. In PFD-treated PCCs, expression of p21 was increased but that of CDK2 was not clearly decreased. Of note, PFD did not induce significant apoptosis among PCCs. Conclusions: These results demonstrated that the antifibrotic agent PFD might have antiproliferative effects on PCCs by inducing G0/G1 cell cycle arrest. This suggests that PFD may target not only fibroblasts but also PCCs in the tumor microenvironment of pancreatic cancer.

Thymosin alpha 1 stimulates cell proliferation by activating ERK1/2 and JNK and increasing cytokine secretion in human pancreatic cancer cells

2006 ◽  
Vol 130 (2) ◽  
pp. 264
Author(s):  
M. Li ◽  
L. Feurino ◽  
F. Li ◽  
W.E. Fisher ◽  
C. Chen ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cytokine Secretion ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Thymosin Alpha 1

Protease-activated receptor-2 regulates cell proliferation and enhances cyclooxygenase-2 mRNA expression in human pancreatic cancer cells

2005 ◽  
Vol 89 (2) ◽  
pp. 79-85 ◽  
Author(s):  
Kazuhiro Yada ◽  
Kohei Shibata ◽  
Toshifumi Matsumoto ◽  
Masayuki Ohta ◽  
Shigeo Yokoyama ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Cyclooxygenase 2 ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Protease Activated Receptor 2

Interleukin-8 gene silencing on pancreatic cancer cells using biodegradable polymer nanoplexes

2014 ◽  
Vol 2 (7) ◽  
pp. 1007-1015 ◽  
Author(s):  
Guimiao Lin ◽  
Chengbin Yang ◽  
Rui Hu ◽  
Chih-Kuang Chen ◽  
Wing-Cheung Law ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Gene Silencing ◽  
Cancer Cells ◽  
Biodegradable Polymer ◽  
Interleukin 8 ◽  
Pancreatic Cancer Cells

Biodegradable polymer nanoplexes were used as siRNA carriers for interleukin-8 gene silencing to attenuate cell proliferation in pancreatic cancer cells.

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