Potential role of KLF10 in the regulation of gemcitabine resistance in pancreatic cancer cells

Pancreatology ◽  
2012 ◽  
Vol 12 (6) ◽  
pp. 510-511
Author(s):  
Mei-Ren Pan ◽  
Li-Tzong Chen ◽  
Wen-Chun Hung
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Potential Role ◽  
Gemcitabine Resistance ◽  
Pancreatic Cancer Cells

scholarly journals Linc-DYNC2H1-4 promotes EMT and CSC phenotypes by acting as a sponge of miR-145 in pancreatic cancer cells

2017 ◽  
Vol 8 (7) ◽  
pp. e2924-e2924 ◽  
Author(s):  
Yuran Gao ◽  
Zhicheng Zhang ◽  
Kai Li ◽  
Liying Gong ◽  
Qingzhu Yang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Ectopic Expression ◽  
Pancreatic Cancer Cell Line ◽  
Mesenchymal Transition ◽  
Gemcitabine Resistance ◽  
Pancreatic Cancer Cells ◽  
Sense Strand ◽  
The Impact

AbstractThe acquisition of epithelial–mesenchymal transition (EMT) and/or existence of a sub-population of cancer stem-like cells (CSC) are associated with malignant behavior and chemoresistance. To identify which factor could promote EMT and CSC formation and uncover the mechanistic role of such factor is important for novel and targeted therapies. In the present study, we found that the long intergenic non-coding RNA linc-DYNC2H1-4 was upregulated in pancreatic cancer cell line BxPC-3-Gem with acquired gemcitabine resistance. Knockdown of linc-DYNC2H1-4 decreased the invasive behavior of BxPC-3-Gem cells while ectopic expression of linc-DYNC2H1-4 promoted the acquisition of EMT and stemness of the parental sensitive cells. Linc-DYNC2H1-4 upregulated ZEB1, the EMT key player, which led to upregulation and downregulation of its targets vimentin and E-cadherin respectively, as well as enhanced the expressions of CSC makers Lin28, Nanog, Sox2 and Oct4. Linc-DYNC2H1-4 is mainly located in the cytosol. Mechanically, it could sponge miR-145 that targetsZEB1,Lin28,Nanog,Sox2,Oct4to restore these EMT and CSC-associated genes expressions. We proved thatMMP3, the nearby gene of linc-DYNC2H1-4 in the sense strand, was also a target of miR-145. Downregulation ofMMP3by miR-145 was reverted by linc-DYNC2H1-4, indicating that competing with miR-145 is one of the mechanisms for linc-DYNC2H1-4 to regulateMMP3. In summary, our results explore the important role of linc-DYNC2H1-4 in the acquisition of EMT and CSC, and the impact it has on gemcitabine resistance in pancreatic cancer cells.

Potential role of acid ceramidase in conversion of cytostatic to cytotoxic end-point in pancreatic cancer cells

2012 ◽  
Vol 71 (3) ◽  
pp. 635-645 ◽  
Author(s):  
Samy A. F. Morad ◽  
Maria C. Messner ◽  
Jonathan C. Levin ◽  
Noha Abdelmageed ◽  
Hyejung Park ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Potential Role ◽  
Acid Ceramidase ◽  
End Point ◽  
Pancreatic Cancer Cells

A potential role of calpains in sulfonylureas (SUs) –mediated death of human pancreatic cancer cells (1.2B4)

2021 ◽  
pp. 105128
Author(s):  
Izabela Szymczak-Pajor ◽  
Krzysztof Fleszar ◽  
Jacek Kasznicki ◽  
Patrycja Gralewska ◽  
Agnieszka Śliwińska
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Potential Role ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells

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 Bitter melon juice targets molecular mechanisms underlying gemcitabine resistance in pancreatic cancer cells

2015 ◽  
Vol 46 (4) ◽  
pp. 1849-1857 ◽  
Author(s):  
RANGANATHA R. SOMASAGARA ◽  
GAGAN DEEP ◽  
SANGEETA SHROTRIYA ◽  
MANISHA PATEL ◽  
CHAPLA AGARWAL ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Bitter Melon ◽  
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.

The Role of Oxygen-Derived Free Radicals and Nitric Oxide in Cytokine-Induced Antiproliferation of Pancreatic Cancer Cells

Pancreas ◽  
2002 ◽  
Vol 24 (2) ◽  
pp. 161-168 ◽  
Author(s):  
William J. Thomas ◽  
Deborah L. Thomas ◽  
Joseph A. Knezetic ◽  
Thomas E. Adrian
Keyword(s):  
Nitric Oxide ◽  
Pancreatic Cancer ◽  
Free Radicals ◽  
Cancer Cells ◽  
Pancreatic Cancer Cells ◽  
Oxygen Derived Free Radicals
Sign in / Sign up

Export Citation Format

Share Document