Transfection of antisense oligodeoxynucleotide inhibits heparanase gene expression and invasive ability of human pancreatic cancer cellin vitro

2006 ◽  
Vol 26 (1) ◽  
pp. 72-74 ◽  
Author(s):  
Gao Jun ◽  
Su Lin ◽  
Qin Renyi ◽  
Chang Qing ◽  
Huang Tao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Human Pancreatic Cancer ◽  
Antisense Oligodeoxynucleotide ◽  
Invasive Ability

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 Local and Systemic Cytokine Profiling for Pancreatic Ductal Adenocarcinoma to Study Cancer Cachexia in an Era of Precision Medicine

2018 ◽  
Vol 19 (12) ◽  
pp. 3836 ◽  
Author(s):  
Michael H. Gerber ◽  
Patrick W. Underwood ◽  
Sarah M. Judge ◽  
Daniel Delitto ◽  
Andrea E. Delitto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cancer Cachexia ◽  
Soluble Proteins ◽  
Triceps Surae ◽  
Human Pancreatic Cancer ◽  
Ductal Adenocarcinoma ◽  
Related Gene ◽  
Pdx Models

Cancer cachexia is a debilitating condition seen frequently in patients with pancreatic ductal adenocarcinoma (PDAC). The underlying mechanisms driving cancer cachexia are not fully understood but are related, at least in part, to the immune response to the tumor both locally and systemically. We hypothesize that there are unique differences in cytokine levels in the tumor microenvironment and systemic circulation between PDAC tumors and that these varying profiles affect the degree of cancer cachexia observed. Patient demographics, operative factors, oncologic factors, and perioperative data were collected for the two patients in the patient derived xenograft (PDX) model. Human pancreatic cancer PDX were created by implanting fresh surgical pancreatic cancer tissues directly into immunodeficient mice. At PDX end point, mouse tumor, spleen and muscle tissues were collected and weighed, muscle atrophy related gene expression measured, and tumor and splenic soluble proteins were analyzed. PDX models were created from surgically resected patients who presented with different degrees of cachexia. Tumor free body weight and triceps surae weight differed significantly between the PDX models and control (P < 0.05). Both PDX groups had increased atrophy related gene expression in muscle compared to control (FoxO1, Socs3, STAT3, Acvr2b, Atrogin-1, MuRF1; P < 0.05). Significant differences were noted in splenic soluble protein concentrations in 14 of 15 detected proteins in tumor bearing mice when compared to controls. Eight splenic soluble proteins were significantly different between PDX groups (P < 0.05). Tumor soluble proteins were significantly different between the two PDX groups in 15 of 24 detected proteins (P < 0.05). PDX models preserve the cachectic heterogeneity found in patients and are associated with unique cytokine profiles in both the spleen and tumor between different PDX. These data support the use of PDX as a strategy to study soluble cachexia protein markers and also further efforts to elucidate which cytokines are most related to cachexia in order to provide potential targets for immunotherapy.

Differential gene expression of the key signalling pathway in para-carcinoma, carcinoma and relapse human pancreatic cancer

2013 ◽  
Vol 32 (3) ◽  
pp. 258-267 ◽  
Author(s):  
Zheng-Yan Chang ◽  
Ran Sun ◽  
Yu-Shui Ma ◽  
Da Fu ◽  
Xiao-Long Lai ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Differential Gene Expression ◽  
Signalling Pathway ◽  
Human Pancreatic Cancer ◽  
Differential Gene

scholarly journals Growth of Human Pancreatic Cancer Is Inhibited by Down-Regulation of Gastrin Gene Expression

Pancreas ◽  
2009 ◽  
Vol 38 (5) ◽  
pp. e151-e161 ◽  
Author(s):  
Gail L. Matters ◽  
John F. Harms ◽  
Christopher O. McGovern ◽  
Calpurnia Jayakumar ◽  
Keisha Crepin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Human Pancreatic Cancer ◽  
Down Regulation

ING3 as a novel regulator of pancreatic cancer growth and aggressiveness.

2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 304-304
Author(s):  
Marina Koutsioumpa ◽  
Maria Hatziapostolou ◽  
Christos Polytarchou ◽  
Swapna Joshi ◽  
Dimitrios Iliopoulos
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Cell Lines ◽  
Colony Formation ◽  
Genetic Alterations ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cell ◽  
Qrt Pcr ◽  
Chromatin Regulators

304 Background: Recent studies demonstrate that chromatin regulation by posttranslational means, such as histone methylation or acetylation, is an essential control mechanism in tumorigenesis and tumor progression. Accumulative findings support the notion that pancreatic cancer tumorigenesis is not only governed by genetic alterations but also aberrant epigenetic regulation. The aim of the present study was to identify and assess the role of chromatin regulators in pancreatic cancer. Methods: The gene expression profile of chromatin regulators was assessed using gene expression microarray analysis in pancreatic cancer and uninvolved human tissues. Validation of microarray findings was performed by qRT-PCR in two extended cohorts of patients and by immunohistochemistry in pancreas tumor tissue microarrays. PANC-1, MIA Paca-2, Capan-2, HPAF-II and AsPC-1 cell lines were used for in vitro assays. Efficiency of knockdown experiments, performed by RNAi interference assays and shRNA-expressing lentiviral vectors, was evidenced by qRT-PCR and Western Blot Analysis. Cell proliferation, invasion and colony formation assays were conducted in genetically modified cells. The significance of variability between the results from each group and corresponding control was determined by unpaired t-test. Results: Differential expression analysis of chromatin regulators in pancreatic cancer versus uninvolved tissues demonstrates that 27 epigenetic molecules are significantly de-regulated (>1.5 fold, P<0.05). By hierarchical clustering, the samples are classified into two major groups that reflect the normal and cancer state. The decreased expression of inhibitor of growth family member 3 (ING3), a component of the NuA4 histone acetyl-transferase complex, was further validated by qRT-PCR and immunohistochemistry analysis in tumor tissues. Transient or stable silencing of ING3 caused significant increase of viability, proliferation, colony formation and invasion in several pancreatic cell lines. Conclusions: Our data show that human pancreatic cancer is characterized by loss of ING3 expression and we defined a potential role of the latter in pancreatic cancer cell growth and invasion.

scholarly journals In VitroGlobal Gene Expression Analyses Support the Ethnopharmacological Use ofAchyranthes aspera

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Pochi R. Subbarayan ◽  
Malancha Sarkar ◽  
Lubov Nathanson ◽  
Nikesh Doshi ◽  
Balakrishna L. Lokeshwar ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Mode Of Action ◽  
Gene Expression Regulation ◽  
Pancreatic Cancer Cell Line ◽  
Human Pancreatic Cancer ◽  
Anticancer Properties ◽  
Thomson Reuters ◽  
Gene Expression Analyses

Achyranthes aspera(familyAmaranthaceae) is known for its anticancer properties. We have systematically validated thein vitroandin vivoanticancer properties of this plant. However, we do not know its mode of action. Global gene expression analyses may help decipher its mode of action. In the absence of identified active molecules, we believe this is the best approach to discover the mode of action of natural products with known medicinal properties. We exposed human pancreatic cancer cell line MiaPaCa-2 (CRL-1420) to 34 μg/mL of LE for 24, 48, and 72 hours. Gene expression analyses were performed using whole human genome microarrays (Agilent Technologies, USA). In our analyses, 82 (54/28) genes passed the quality control parameter, set at FDR ≤ 0.01 and FC of ≥±2. LE predominantly affected pathways of immune response, metabolism, development, gene expression regulation, cell adhesion, cystic fibrosis transmembrane conductance regulation (CFTR), and chemotaxis (MetaCore tool (Thomson Reuters, NY)). Disease biomarker enrichment analysis identified LE regulated genes involved in Vasculitis—inflammation of blood vessels. Arthritis and pancreatitis are two of many etiologies for vasculitis. The outcome of disease network analysis supports the medicinal use ofA. aspera, viz, to stop bleeding, as a cure for pancreatic cancer, as an antiarthritic medication, and so forth.

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