Growth inhibition of human pancreatic cancer cells by cholecystokinin receptor antagonist in tissue culture and in nude mice

1992 ◽  
Vol 27 (1) ◽  
pp. 78-82 ◽  
Author(s):  
Akihiro Funakoshi ◽  
Akira Kono
Keyword(s):  
Pancreatic Cancer ◽  
Tissue Culture ◽  
Growth Inhibition ◽  
Receptor Antagonist ◽  
Cancer Cells ◽  
Nude Mice ◽  
Human Pancreatic Cancer ◽  
Cholecystokinin Receptor ◽  
Pancreatic Cancer Cells

scholarly journals The dominant negative H-ras mutant, N116Y, suppresses growth of metastatic human pancreatic cancer cells in the liver of nude mice

Gene Therapy ◽  
2000 ◽  
Vol 7 (6) ◽  
pp. 518-526 ◽  
Author(s):  
M Takeuchi ◽  
T Shichinohe ◽  
N Senmaru ◽  
M Miyamoto ◽  
H Fujita ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Nude Mice ◽  
Dominant Negative ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells

scholarly journals Brusatol Enhances the Chemotherapy Efficacy of Gemcitabine in Pancreatic Cancer via the Nrf2 Signalling Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yukai Xiang ◽  
Wen Ye ◽  
Chaohao Huang ◽  
Dinglai Yu ◽  
Hao Chen ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Advanced Pancreatic Cancer ◽  
Signalling Pathway ◽  
Human Pancreatic Cancer ◽  
Control Treatment ◽  
Nrf2 Pathway ◽  
Pancreatic Cancer Cells ◽  
Nrf2 Activation

Although gemcitabine is the standard chemotherapy treatment for advanced pancreatic cancer, its benefits are quite limited due to prevalent chemoresistance, and the mechanism underlying gemcitabine chemoresistance remains unclear. Currently, Nrf2 has been deemed as a significant contributor to gemcitabine chemoresistance in pancreatic cancer. Brusatol is a unique inhibitor of the Nrf2 pathway, and in previous studies, we determined that brusatol exhibits the effects of growth inhibition and proapoptosis in pancreatic cancer cells. Due to these data, we speculate that brusatol can reverse gemcitabine-induced Nrf2 activation and propose that it can enhance gemcitabine efficacy in treating pancreatic cancer. In this study, we first proved that brusatol can effectively inhibit the Nrf2 signalling pathway and increase ROS accumulation in pancreatic cancer cells. Next, we demonstrated that brusatol can abrogate gemcitabine-induced Nrf2 activation in pancreatic cancer cells. In addition, we discovered that brusatol potentiates gemcitabine-induced growth inhibition and apoptosis in human pancreatic cancer cells. In nude mice with PANC-1 xenografts, treatment with a combination of brusatol and gemcitabine considerably reduced in vivo tumour growth compared with control treatment or treatment with either brusatol or gemcitabine alone. Immunohistochemical staining also showed that Nrf2 expression levels were reduced in brusatol-treated xenograft tumour tissues. In summary, our results suggest that brusatol is capable of enhancing the antitumour effects of gemcitabine in both pancreatic cancer cells and PANC-1 xenografts via suppressing the Nrf2 pathway.

Identification of gastrin as a growth peptide in human pancreatic cancer

1995 ◽  
Vol 268 (1) ◽  
pp. R135-R141 ◽  
Author(s):  
J. P. Smith ◽  
A. P. Fantaskey ◽  
G. Liu ◽  
I. S. Zagon
Keyword(s):  
Pancreatic Cancer ◽  
Receptor Antagonist ◽  
Nude Mice ◽  
Binding Capacity ◽  
Human Tumor ◽  
Human Pancreatic Cancer ◽  
Athymic Nude Mice ◽  
Cells In Culture ◽  
Pancreatic Cancer Cells ◽  
Regulation Of Growth

The present study reports the first evidence that the gastrointestinal peptide gastrin stimulates the growth of several human pancreatic cancer cells in culture and in tumors transplanted to nude mice. Gastrin promoted growth of all cell lines tested at a dose comparable to the binding affinity, providing evidence for a physiologically relevant receptor. The stimulatory effects of gastrin were blocked by the CCK-B/gastrin receptor antagonist L-365,260 and not by the CCK-A receptor antagonist L-364,718. Growth of PANC-1 cells in culture were inhibited by L-365,260, suggesting that gastrin is tonically produced by PANC-1 cells for regulation of growth. Athymic nude mice bearing PANC-1 xenografts were treated for 24 days subcutaneously with either 1% bovine serum albumin (diluent), pentagastrin (1 mg/kg), or L-365,260 (1 mg/kg) twice daily. Tumors from the pentagastrin-treated mice were found to weigh more and have greater protein and DNA content than controls, whereas these values were all decreased in tumors of L-365,260-treated mice. Receptor binding capacity changed in tumors of animals treated with the peptide or antagonist, suggesting a regulatory process. Gastrin immunoreactivity was detected in a transplanted PANC-1 human tumor. These results identify gastrin as a potent trophic peptide that actively stimulates growth of human pancreatic cancer and does so through a CCK-B/gastrin-like receptor.

Cholecystokinin receptors and PANC-1 human pancreatic cancer cells

1993 ◽  
Vol 265 (1) ◽  
pp. G149-G155 ◽  
Author(s):  
J. P. Smith ◽  
C. A. Rickabaugh ◽  
P. J. McLaughlin ◽  
I. S. Zagon
Keyword(s):  
Pancreatic Cancer ◽  
Receptor Antagonist ◽  
Cancer Cells ◽  
Binding Capacity ◽  
Pancreatic Cancer Cell Line ◽  
Human Pancreatic Cancer ◽  
Scatchard Analysis ◽  
Binding Studies ◽  
Cck Receptors ◽  
Pancreatic Cancer Cells

The gastrointestinal peptide cholecystokinin (CCK) has been shown to stimulate growth of human pancreatic adenocarcinoma in vitro and in vivo, although CCK receptors have not been identified in pancreatic cancer cells. The purpose of this study was to characterize the CCK receptors in pancreatic cancer cells and to correlate the receptor binding studies with the trophic action of CCK agonists and antagonists. With the use of homogenates of PANC-1 human pancreatic cancer cell line grown in culture, the binding of 125I-labeled CCK octapeptide (125I-CCK-8) was examined under various conditions to characterize the CCK receptor. Specific and saturable binding of 125I-CCK-8 was detected in PANC-1 cells; data were consistent with a single binding site. Scatchard analysis yielded a binding affinity [dissociation constant (Kd)] of 2.8 nM and a binding capacity of 26 fmol/mg protein. Binding was dependent on protein concentration, time, temperature, the presence of protease inhibitors, and pH and was sensitive to Na+, K+, Mg2+, and ethylene glycolbis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. Competition experiments indicated that L-365,260, a selective CCK-B (gastrin) receptor antagonist, was the most potent displacer of 125I-CCK-8, and no significant displacement of binding was found with the selective CCK-A receptor antagonist. Growth of PANC-1 cells in culture was stimulated by CCK at a concentration consistent with the Kd, and CCK-stimulated growth was inhibited by the CCK-B receptor antagonist (L-365,260) not the CCK-A receptor antagonist (L-364,718).(ABSTRACT TRUNCATED AT 250 WORDS)

KLF8 knockdown triggered growth inhibition and induced cell phase arrest in human pancreatic cancer cells

Gene ◽  
2016 ◽  
Vol 585 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Xiaoping Yi ◽  
Yixiong Li ◽  
Hongyan Zai ◽  
Xueying Long ◽  
Wenzheng Li
Keyword(s):  
Pancreatic Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Phase Arrest
Sign in / Sign up

Export Citation Format

Share Document