scholarly journals Expression of KLF9 in pancreatic cancer and its effects on the invasion, migration, apoptosis, cell cycle distribution, and proliferation of pancreatic cancer cell lines

2018 ◽  
Author(s):  
Zhiwei Zhong ◽  
Fan Zhou ◽  
Dong Wang ◽  
Mingming Wu ◽  
Weimin Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Cell Cycle Distribution

Identifying Functional Differences Between Protein S and Gas-6 in Pancreatic Cancer

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2571-2571
Author(s):  
Cosette Zacarias ◽  
Vijaya Satish Sekhar Pilli ◽  
William E. Plautz ◽  
A'drianne Wells ◽  
Rinku Majumder
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Biology ◽  
Pancreatic Cancer Cell ◽  
Protein S ◽  
Cancer Cell Lines ◽  
Cancer Cell Proliferation

Abstract Introduction: Procoagulants such as Factor IX and thrombin play major roles in cancer cell proliferation and migration; however, a role for anticoagulant proteins in cancer biology has not been elucidated. The anticoagulant Protein S (PS), its homologous protein Growth Arrest Specific protein-6 (GAS-6), and the receptors for these proteins, Tyro-3, Axl and Mertk (TAM), are over expressed in many cancer cells. TAM family receptors regulate functions such as cell survival, proliferation, migration, and apoptosis. The consequences of activation of each of these receptors varies, although the mechanism that leads to different outcomes is unknown. We hypothesized that the PS and GAS-6 ligands are responsible for the variations in the functions of these signaling cascades. Methods: We used qPCR to analyze the pancreatic cancer cell lines Miapaca-2 and Panc-1 for variations in the expression of GAS-6 and PS. We sequestered PS and GAS-6 with antibodies and used FACS analysis to detect effects on the cell cycle and on cell cycle regulators. Results: GAS-6 was observed to be highly expressed in proliferating Miapaca-2 cells compared with Panc-1 cells, whereas there was no significant difference in PS mRNA levels between these cell lines. For the cell line Miapaca-2, antibody sequestration of GAS-6 arrested the cell cycle in S-phase and increased p53 phosphorylation; conversely, inhibition of PS reduced p53 phosphorylation. Conclusion: Our results indicate that PS and GAS-6 act antagonistically in controlling pancreatic cancer cell proliferation, and we hypothesize that the ratio of GAS-6 to PS expression is key to this regulation. We will further confirm our hypothesis by overexpressing and knocking down PS and GAS-6 in the pancreatic cancer cell lines. Disclosures No relevant conflicts of interest to declare.

Biglycan induced growth inhibition in pancreatic cancer cell lines is caused by cell cycle arrest in G1

2000 ◽  
Vol 118 (4) ◽  
pp. A541
Author(s):  
Gerrit Sommer ◽  
Martina Weimer ◽  
Uli Lacher ◽  
Claudia Ruhland ◽  
Christoph Wenger ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Growth Inhibition ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Cycle Arrest

Ritonavir mediated protection of retinoblastoma-E2F-1 complex at G1 phase of cell cycle in pancreatic cancer cell lines

2008 ◽  
Vol 207 (3) ◽  
pp. S97
Author(s):  
Ramesh B. Batchu ◽  
Madhu Prasad ◽  
Chris Steffes ◽  
Masood Shammas ◽  
Basil F. El-Rayes ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
G1 Phase

Effect of a combination of S-1 and gemcitabine on cell cycle regulation in pancreatic cancer cell lines

2012 ◽  
Vol 23 (5) ◽  
pp. 505-514 ◽  
Author(s):  
Yoshihito Morimoto ◽  
Osamu Takeuchi ◽  
Asako Takizawa ◽  
Hiroshi Yoneyama ◽  
Fumiki Asanuma ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Cycle Regulation ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Cycle Regulation

Gastrin regulates growth of human pancreatic cancer in a tonic and autocrine fashion

1996 ◽  
Vol 270 (5) ◽  
pp. R1078-R1084 ◽  
Author(s):  
J. P. Smith ◽  
A. Shih ◽  
Y. Wu ◽  
P. J. McLaughlin ◽  
I. S. Zagon
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Human Pancreatic Cancer ◽  
Growth Media ◽  
Human Pancreatic Cancer Cell ◽  
Cell Extracts

The gastrointestinal peptides gastrin and cholecystokinin (CCK) stimulate growth of human pancreatic cancer through a CCK-B/gastrin- like receptor. In the present study we evaluated whether growth of human pancreatic cancer is endogenously regulated by gastrin. Immunohistomical examination of BxPC-3 cells and tumor xenografts revealed specifc gastrin immunoreactivity. Gastrin was detected by radioimmunoassay in pancreatic cancer cell extracts and in pancreatic cancer cell extracts and in the growth media. With use of reverse-transcriptase polymerase chain reaction gastrin gene expression was detected in both cultured BxPC-3 cancer cells and transplanted tumors, as well as seven addition human pancreatic cancer cell lines. Growth of BxPC-3 human pancreatic cancer cell in serum-free medium was inhibited by the addition of the CCK-B/gastrin receptor antagonist L-365,260, and gastrin treatment reversed the inhibitory effect of the antagonist. A selective gastrin antibody (Ab repressed growth of BxPC-3 cells. Gastrin immunoreactivity was detected in fresh human pancreatic cancer specimens but not in normal human pancreatic tissue. These data provide the first evidence that growth of a human pancreatic cancer is tonically stimulated by the autocrine production of gastrin. Evidence for the ubiquity of this system was provided by the detection of gastrin gene expression in multiple human pancreatic cancer cell lines and detection of gastrin in cell lines and fresh pancreatic tumors.

scholarly journals Verteporfin-based photodynamic therapy overcomes gemcitabine insensitivity in a panel of pancreatic cancer cell lines

2011 ◽  
Vol 43 (7) ◽  
pp. 565-574 ◽  
Author(s):  
Jonathan P. Celli ◽  
Nicolas Solban ◽  
Alvin Liang ◽  
Stephen P. Pereira ◽  
Tayyaba Hasan
Keyword(s):  
Pancreatic Cancer ◽  
Photodynamic Therapy ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines

scholarly journals OSU-A9 inhibits pancreatic cancer cell lines by modulating p38-JAK-STAT3 signaling

Oncotarget ◽  
2017 ◽  
Vol 8 (17) ◽  
pp. 29233-29246 ◽  
Author(s):  
Wan-Chi Tsai ◽  
Li-Yuan Bai ◽  
Yi-Jin Chen ◽  
Po-Chen Chu ◽  
Ya-Wen Hsu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Stat3 Signaling
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