Differential proteomic analysis of pancreatic cancer cell-derived exosomes provides new insights into cancer metastasis and novel biomarkers for early detection

Pancreatology ◽  
2017 ◽  
Vol 17 (4) ◽  
pp. S23 ◽  
Author(s):  
Haoyi Jin ◽  
Xiaodong Tan
Keyword(s):  
Pancreatic Cancer ◽  
Early Detection ◽  
Cancer Cell ◽  
Proteomic Analysis ◽  
Cancer Metastasis ◽  
Pancreatic Cancer Cell ◽  
Novel Biomarkers

scholarly journals ELMO2 association with Gαi2 regulates pancreatic cancer cell chemotaxis and metastasis

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8910
Author(s):  
Yecheng Wang ◽  
Hongyan Li ◽  
Fei Li
Keyword(s):  
Pancreatic Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Actin Polymerization ◽  
Molecular Mechanisms ◽  
Cancer Metastasis ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Migration ◽  
Pancreatic Cancer Cells ◽  
Cell Chemotaxis

Background Pancreatic cancer is a highly lethal disease. Nearly half of the patients have distant metastasis and remain asymptomatic. Emerging evidence suggests that the chemokine, CXCL12, has a role in cancer metastasis. The interaction between CXCL12 and CXCR4 activates heterotrimeric G proteins, which regulates actin polymerization and cancer cell migration. However, the molecular mechanisms underlying pancreatic cancer cell migration are still largely obscure. Here, we addressed the role of ELMO2 in chemotaxis and metastasis of pancreatic cancer cells. Methods Pancreatic cancer cell lines PANC-1 and AsPC-1 and siRNA-mediated knockdown of ELMO2 were used to determine the effects of ELMO2 on cancer cell chemotaxis, invasion, migration. Co-immunoprecipitation assays were carried out to identify interacting partners of ELMO2. Results ELMO2 knockdown inhibited pancreatic cancer cell chemotaxis, migration, invasion, and F-actin polymerization. Co-immunoprecipitation assays revealed that ELMO2 interacted with Gαi2 and that CXCL12 triggered Gα i2-dependent membrane translocation of ELMO2. Thus, ELMO2 is a potential therapeutic target for pancreatic cancer.

Ligation of fas antigen stimulates chemoline secretion in pancreatic cancer cell line PANC-1

2001 ◽  
Vol 120 (5) ◽  
pp. A336-A336
Author(s):  
M SHIMADA ◽  
A ANDOH ◽  
Y ARAKI ◽  
Y FUJIYAMA ◽  
T BAMBA
Keyword(s):  
Pancreatic Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Pancreatic Cancer Cell Line ◽  
Cancer Cell Line ◽  
Fas Antigen

Zinc chelator TPEN induces pancreatic cancer cell death through causing oxidative stress and inhibiting cell autophagy

2019 ◽  
Vol 234 (11) ◽  
pp. 20648-20661 ◽  
Author(s):  
Zhen Yu ◽  
Ze Yu ◽  
ZhenBao Chen ◽  
Lin Yang ◽  
MingJun Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Cancer ◽  
Cell Death ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Death ◽  
Zinc Chelator

scholarly journals Forkhead box B2 inhibits the malignant characteristics of the pancreatic cancer cell line Panc‐1 in vitro

2019 ◽  
Vol 24 (10) ◽  
pp. 674-681
Author(s):  
Hiroki Fukuchi ◽  
Yukinobu Hayashida ◽  
Kunio Inoue ◽  
Yoshifusa Sadamura
Keyword(s):  
Pancreatic Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Pancreatic Cancer Cell Line ◽  
Cancer Cell Line ◽  
Forkhead Box

Devil’s Club Falcarinol-Type Polyacetylenes Inhibit Pancreatic Cancer Cell Proliferation

2019 ◽  
Vol 71 (2) ◽  
pp. 301-311 ◽  
Author(s):  
Susan S. C. Cheung ◽  
David Hasman ◽  
Djamel Khelifi ◽  
Joseph Tai ◽  
Richard W. Smith ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Proliferation

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.

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