Integrated analysis of gene expression and methylation profiles of novel pancreatic cancer cell lines with highly metastatic activity

2019 ◽  
Vol 62 (6) ◽  
pp. 791-806 ◽  
Author(s):  
Gang Yang ◽  
Huanyu Wang ◽  
Mengyu Feng ◽  
Lei You ◽  
Lianfang Zheng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Integrated Analysis ◽  
Metastatic Activity

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.

GENE EXPRESSION PROFILING DISTINGUISHES BETWEEN DRUG-SENSITIVE AND RESISTANT PANCREATIC CANCER CELL LINES

Pancreas ◽  
2008 ◽  
Vol 37 (4) ◽  
pp. 460
Author(s):  
T. Arumugam ◽  
W. Choi ◽  
V. Ramachandran ◽  
K. F. Fournier ◽  
G. E. Gallick ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Gene Expression Profiling ◽  
Cell Lines ◽  
Cancer Cell ◽  
Expression Profiling ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines

Frequent loss of RUNX3 gene expression in human bile duct and pancreatic cancer cell lines

2003 ◽  
Vol 124 (4) ◽  
pp. A287
Author(s):  
Manabu Wada ◽  
Shojiro Yazumi ◽  
Shigeo Takaishi ◽  
Kazunori Hasegawa ◽  
Mitsutaka ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Bile Duct ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Human Bile ◽  
Runx3 Gene

scholarly journals Genomic Profiling and Functional Analysis of let-7c miRNA-mRNA Interactions Identify SOX13 to Be Involved in Invasion and Progression of Pancreatic Cancer

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Shannon R. Nelson ◽  
Sandra Roche ◽  
Maura Cotter ◽  
Pablo Anton Garcia ◽  
Daniela Reitmeier ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Differential Expression ◽  
Cell Lines ◽  
Cancer Cell ◽  
Colony Formation ◽  
Normal Tissue ◽  
Target Genes ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Integrated Analysis

Background. Pancreatic cancer is a devastating disease; its lethality is related to rapid growth and tendency to invade adjacent organs and metastasize at an early stage. Objective. The aim of this study was to identify miRNAs and their gene targets involved in the invasive phenotype in pancreatic cancer to better understand the biological behaviour and the rapid progression of this disease. Methods. miRNA profiling was performed in isogenic matched high invasive and low-invasive subclones derived from the MiaPaCa-2 cell line and validated in a panel of pancreatic cancer cell lines, tumour, and normal pancreas. Online miRNA target prediction algorithms and gene expression arrays were used to predict the target genes of the differentially expressed miRNAs. miRNAs and potential target genes were subjected to overexpression and knockdown approaches and downstream functional assays to determine their pathological role in pancreatic cancer. Results. Differential expression analysis revealed 10 significantly dysregulated miRNAs associated with invasive capacity (Student’s t-tests; P value <0.05; fold change = ±2). The expression of top upregulated miR-135b and downregulated let-7c miRNAs correlated with the invasive abilities of eight pancreatic cancer cell lines and displayed differential expression in pancreatic cancer and adjacent normal tissue specimens. Ectopic overexpression of let-7c decreased proliferation, invasion, and colony formation. Integrated analysis of miRNA-mRNA using in silico algorithms and experimental validation databases identified four putative gene targets of let-7c. One of these targets, SOX13, was found to be upregulated in PDAC tumour compared with normal tissue in TCGA and an independent data set by qPCR and immunohistochemistry. RNAi knockdown of SOX13 reduced the invasion and colony formation ability of pancreatic cancer cells. Conclusion. The identification of key miRNA-mRNA gene interactions and networks provide potential diagnostic and therapeutic strategies for better treatment options for pancreatic cancer patients.

scholarly journals Histone deacetylase (HDAC) encoding gene expression in pancreatic cancer cell lines and cell sensitivity to HDAC inhibitors

2008 ◽  
Vol 7 (4) ◽  
pp. 523-531 ◽  
Author(s):  
M. Ouaïssi ◽  
S. Cabral ◽  
J. Tavares ◽  
A. Cordeiro da Silva ◽  
F. Mathieu-Daude ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Histone Deacetylase ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Hdac Inhibitors ◽  
Cancer Cell Lines ◽  
Cell Sensitivity ◽  
Encoding Gene

scholarly journals DeltaNp63-dependent super enhancers define molecular identity in pancreatic cancer by an interconnected transcription factor network

2018 ◽  
Vol 115 (52) ◽  
pp. E12343-E12352 ◽  
Author(s):  
Feda H. Hamdan ◽  
Steven A. Johnsen
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Transcriptional Regulatory Network ◽  
Expression Patterns ◽  
Gene Expression Signature ◽  
Cancer Cell Lines ◽  
Precision Oncology

Molecular subtyping of cancer offers tremendous promise for the optimization of a precision oncology approach to anticancer therapy. Recent advances in pancreatic cancer research uncovered various molecular subtypes with tumors expressing a squamous/basal-like gene expression signature displaying a worse prognosis. Through unbiased epigenome mapping, we identified deltaNp63 as a major driver of a gene signature in pancreatic cancer cell lines, which we report to faithfully represent the highly aggressive pancreatic squamous subtype observed in vivo, and display the specific epigenetic marking of genes associated with decreased survival. Importantly, depletion of deltaNp63 in these systems significantly decreased cell proliferation and gene expression patterns associated with a squamous subtype and transcriptionally mimicked a subtype switch. Using genomic localization data of deltaNp63 in pancreatic cancer cell lines coupled with epigenome mapping data from patient-derived xenografts, we uncovered that deltaNp63 mainly exerts its effects by activating subtype-specific super enhancers. Furthermore, we identified a group of 45 subtype-specific super enhancers that are associated with poorer prognosis and are highly dependent on deltaNp63. Genes associated with these enhancers included a network of transcription factors, including HIF1A, BHLHE40, and RXRA, which form a highly intertwined transcriptional regulatory network with deltaNp63 to further activate downstream genes associated with poor survival.

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