scholarly journals A Histone Deacetylase Inhibitor Suppresses Epithelial-Mesenchymal Transition and Attenuates Chemoresistance in Biliary Tract Cancer

PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0145985 ◽  
Author(s):  
Takuya Sakamoto ◽  
Shogo Kobayashi ◽  
Daisaku Yamada ◽  
Hiroaki Nagano ◽  
Akira Tomokuni ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Biliary Tract ◽  
Biliary Tract Cancer ◽  
Histone Deacetylase Inhibitor ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tract Cancer ◽  
Deacetylase Inhibitor

Hypoxia-Induced PLOD2 is a Key Regulator in Epithelial-Mesenchymal Transition and Chemoresistance in Biliary Tract Cancer

2018 ◽  
Vol 25 (12) ◽  
pp. 3728-3737 ◽  
Author(s):  
Yuichiro Okumura ◽  
Takehiro Noda ◽  
Hidetoshi Eguchi ◽  
Takuya Sakamoto ◽  
Yoshifumi Iwagami ◽  
...  
Keyword(s):  
Biliary Tract ◽  
Biliary Tract Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tract Cancer

scholarly journals MiR-200c-3p Modulates Cisplatin Resistance in Biliary Tract Cancer by ZEB1-Independent Mechanisms

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 3996
Author(s):  
Florian Posch ◽  
Felix Prinz ◽  
Amar Balihodzic ◽  
Christian Mayr ◽  
Tobias Kiesslich ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Biliary Tract ◽  
Biliary Tract Cancer ◽  
Cisplatin Resistance ◽  
Epithelial Mesenchymal Transition ◽  
Gene Expression Pattern ◽  
Underlying Mechanism ◽  
P Value ◽  
Mesenchymal Transition ◽  
Tract Cancer

Biliary tract cancer is a major global health issue in cancer-related mortality. Therapeutic options are limited, and cisplatin-based treatment schedules represent the mainstay of first-line therapeutic strategies. Although the gain of survival by the addition of cisplatin to gemcitabine is moderate, acquired cisplatin resistance frequently leads to treatment failures with mechanisms that are still poorly understood. Epithelial–mesenchymal transition (EMT) is a dynamic process that changes the shape, function, and gene expression pattern of biliary tract cancer cells. In this study, we explored the influence of the EMT-regulating miR-200c-3p on cisplatin sensitivity in biliary tract cancer cells. Using gain of function experiments, we demonstrated that miR-200c-3p regulates epithelial cell markers through the downregulation of the transcription factor ZEB1. MiR-200c-3p upregulation led to a decreased sensitivity against cisplatin, as observed in transient overexpression models as well as in cell lines stably overexpressing miR-200c-3p. The underlying mechanism seems to be independent of miR-200c-3p’s influence on ZEB1 expression, as ZEB1 knockdown resulted in the opposite effect on cisplatin resistance, which was abolished when ZEB1 knockdown and miR-200c-3p overexpression occurred in parallel. Using a gene panel of 40 genes that were previously associated with cisplatin resistance, two (Dual Specificity Phosphatase 16 (DUSP16) and Stratifin (SFN)) were identified as significantly (>2 fold, p-value < 0.05) up-regulated in miR-200c-3p overexpressing cells. In conclusion, miR-200c-3p might be an important contributor to cisplatin resistance in biliary tract cancer, independently of its interaction with ZEB1.

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