The Flavonoid Apigenin Potentiates the Growth Inhibitory Effects of Gemcitabine and Abrogates Gemcitabine Resistance in Human Pancreatic Cancer Cells

Pancreas ◽  
2009 ◽  
Vol 38 (4) ◽  
pp. 409-415 ◽  
Author(s):  
Matthew J. Strouch ◽  
Benjamin M. Milam ◽  
Laleh G. Melstrom ◽  
John J. McGill ◽  
Mohammad R. Salabat ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Inhibitory Effects ◽  
Gemcitabine Resistance ◽  
Pancreatic Cancer Cells ◽  
Growth Inhibitory

scholarly journals Growth-inhibitory effects of vitamin D analogues and retinoids on human pancreatic cancer cells

1996 ◽  
Vol 73 (11) ◽  
pp. 1341-1346 ◽  
Author(s):  
G Zugmaier ◽  
R Jäger ◽  
B Grage ◽  
MM Gottardis ◽  
K Havemann ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Vitamin D ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Inhibitory Effects ◽  
Pancreatic Cancer Cells ◽  
Vitamin D Analogues ◽  
Growth Inhibitory

GROWTH INHIBITORY EFFECTS OF GEMCITABINE ARE AUGMENTED BY THE FLAVONOID APIGENIN IN HUMAN PANCREATIC CANCER CELLS

Pancreas ◽  
2007 ◽  
Vol 35 (4) ◽  
pp. 417
Author(s):  
B. M. Milam ◽  
L. G. Melstrom ◽  
M. J. Strouch ◽  
J. J. McGill ◽  
M. R. Salabat ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Inhibitory Effects ◽  
Pancreatic Cancer Cells ◽  
Growth Inhibitory

scholarly journals Molecular features linked to the growth-inhibitory effects of gemcitabine on human pancreatic cancer cells

2006 ◽  
Author(s):  
Hiroaki Toshimitsu ◽  
Norio Iizuka ◽  
Kohtaro Yamamoto ◽  
Shigeto Kawauchi ◽  
Atsunori Oga ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Inhibitory Effects ◽  
Molecular Features ◽  
Pancreatic Cancer Cells ◽  
Growth Inhibitory

scholarly journals Selenoprotein P, as a predictor for evaluating gemcitabine resistance in human pancreatic cancer cells

2004 ◽  
Vol 112 (2) ◽  
pp. 184-189 ◽  
Author(s):  
Shin-ichiro Maehara ◽  
Shinji Tanaka ◽  
Mitsuo Shimada ◽  
Ken Shirabe ◽  
Yoshiro Saito ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Selenoprotein P ◽  
Gemcitabine Resistance ◽  
Pancreatic Cancer Cells

scholarly journals m6A Methyltransferase METTL14-Mediated Upregulation of Cytidine Deaminase Promoting Gemcitabine Resistance in Pancreatic Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Congjun Zhang ◽  
Shuangyan Ou ◽  
Yuan Zhou ◽  
Pei Liu ◽  
Peiying Zhang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Western Blotting ◽  
Protein Level ◽  
Cytidine Deaminase ◽  
Critical Role ◽  
Human Pancreatic Cancer ◽  
Gemcitabine Resistance ◽  
Pancreatic Cancer Cells

ObjectivePancreatic cancer is one of the most lethal human malignancies. Gemcitabine is widely used to treat pancreatic cancer, and the resistance to chemotherapy is the major difficulty in treating the disease. N6-methyladenosine (m6A) modification, which regulates RNA splicing, stability, translocation, and translation, plays critical roles in cancer physiological and pathological processes. METTL14, an m6A Lmethyltransferase, was found deregulated in multiple cancer types. However, its role in gemcitabine resistance in pancreatic cancer remains elusive.MethodsThe mRNA and protein level of m6A modification associated genes were assessed by QRT-PCR and western blotting. Then, gemcitabine‐resistant pancreatic cancer cells were established. The growth of pancreatic cancer cells were analyzed using CCK8 assay and colony formation assay. METTL14 was depleted by using shRNA. The binding of p65 on METTL14 promoter was assessed by chromatin immunoprecipitation (ChIP) assay. Protein level of deoxycytidine kinase (DCK) and cytidine deaminase (CDA) was evaluated by western blotting. In vivo experiments were conducted to further confirm the critical role of METTL14 in gemcitabine resistance.ResultsWe found that gemcitabine treatment significantly increased the expression of m6A methyltransferase METTL14, and METTL14 was up-regulated in gemcitabine-resistance human pancreatic cancer cells. Suppression of METTL14 obviously increased the sensitivity of gemcitabine in resistant cells. Moreover, we identified that transcriptional factor p65 targeted the promoter region of METTL14 and up-regulated its expression, which then increased the expression of cytidine deaminase (CDA), an enzyme inactivates gemcitabine. Furthermore, in vivo experiment showed that depletion of METTL14 rescue the response of resistance cell to gemcitabine in a xenograft model.ConclusionOur study suggested that METTL14 is a potential target for chemotherapy resistance in pancreatic cancer.

S2015 Growth Inhibitory Effects of Polyphenols in Scutellaria Baicalensis in Pancreatic Cancer Cells

2009 ◽  
Vol 136 (5) ◽  
pp. A-313 ◽  
Author(s):  
Monica C. Chen ◽  
Diane M. Harris ◽  
Qing Y. Lu ◽  
Eliane Angst ◽  
Jenny L. Park ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Scutellaria Baicalensis ◽  
Inhibitory Effects ◽  
Pancreatic Cancer Cells ◽  
Growth Inhibitory

Dimethylamino Parthenolide Enhances the Inhibitory Effects of Gemcitabine in Human Pancreatic Cancer Cells

2012 ◽  
Vol 16 (7) ◽  
pp. 1333-1340 ◽  
Author(s):  
Bryan K. Holcomb ◽  
Michele T. Yip-Schneider ◽  
Joshua A. Waters ◽  
Joal D. Beane ◽  
Peter A. Crooks ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Inhibitory Effects ◽  
Pancreatic Cancer Cells
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