Anti-cancer Activity of Boswellia Carterii Extract Alters the Stress Functional Gene Expression in the Pancreatic Cancer Cell

2019 ◽  
Vol 13 (2) ◽  
pp. 191-201 ◽  
Author(s):  
Yeon-Joo Yoo ◽  
Seong-Eun Huh ◽  
Yumi Kim ◽  
Hyeung-Jin Jang
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Functional Gene ◽  
Anti Cancer ◽  
Boswellia Carterii ◽  
Cancer Activity

Abstract PO-058: Anti-cancer activity of NTAX-44 (bioprocessed arsenic trioxide) on pancreatic cancer cell line

2021 ◽  
Author(s):  
Yogesh Bendale ◽  
Padma Shastri ◽  
Radha Poojari ◽  
Nandinee Khot ◽  
Surendra Nagare ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Line ◽  
Arsenic Trioxide ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Pancreatic Cancer Cell Line ◽  
Cancer Cell Line ◽  
Anti Cancer ◽  
Cancer 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.

scholarly journals Apoptosis-related gene expression profile is changed by gemcitabine in pancreatic cancer cell line (PANC-1)

Suizo ◽  
2007 ◽  
Vol 22 (1) ◽  
pp. 14-20 ◽  
Author(s):  
Takeo SHIMASAKI ◽  
Yasuhito ISHIGAKI ◽  
Toshinari MINAMOTO ◽  
Yoshiharu MOTOO
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Cell Line ◽  
Gene Expression Profile ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Pancreatic Cancer Cell Line ◽  
Cancer Cell Line ◽  
Related Gene ◽  
Apoptosis Related Gene

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

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

scholarly journals C-REV Retains High Infectivity Regardless of the Expression Levels of cGAS and STING in Cultured Pancreatic Cancer Cells

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1502
Author(s):  
Daishi Morimoto ◽  
Shigeru Matsumura ◽  
Itzel Bustos-Villalobos ◽  
Patricia Sibal ◽  
Toru Ichinose ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Human Pancreatic Cancer ◽  
Expression Levels ◽  
Anti Cancer ◽  
Sting Pathway

Oncolytic virus (OV) therapy is widely considered as a major breakthrough in anti-cancer treatments. In our previous study, the efficacy and safety of using C-REV for anti-cancer therapy in patients during stage I clinical trial was reported. The stimulator of interferon genes (STING)–TBK1–IRF3–IFN pathway is known to act as the central cellular host defense against viral infection. Recent reports have linked low expression levels of cGAS and STING in cancer cells to poor prognosis among patients. Moreover, downregulation of cGAS and STING has been linked to higher susceptibility to OV infection among several cancer cell lines. In this paper, we show that there is little correlation between levels of cGAS/STING expression and susceptibility to C-REV among human pancreatic cancer cell lines. Despite having a responsive STING pathway, BxPC-3 cells are highly susceptible to C-REV infection. Upon pre-activation of the STING pathway, BxPc-3 cells exhibited resistance to C-REV infection. However, without pre-activation, C-REV completely suppressed the STING pathway in BxPC-3 cells. Additionally, despite harboring defects in the STING pathway, other high-grade cancer cell lines, such as Capan-2, PANC-1 and MiaPaCa-2, still exhibited low susceptibility to C-REV infection. Furthermore, overexpression of STING in MiaPaCa-2 cells altered susceptibility to a limited extent. Taken together, our data suggest that the cGAS–STING pathway plays a minor role in the susceptibility of pancreatic cancer cell lines to C-REV infection.

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