scholarly journals Growth inhibition of pancreatic cancer cells by histone deacetylase inhibitor belinostat through suppression of multiple pathways including HIF, NFkB, and mTOR signaling in vitro and in vivo

2013 ◽  
Vol 53 (9) ◽  
pp. 722-735 ◽  
Author(s):  
Wenwen Chien ◽  
Dhong Hyun Lee ◽  
Yun Zheng ◽  
Peer Wuensche ◽  
Rosie Alvarez ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitor ◽  
Mtor Signaling ◽  
Pancreatic Cancer Cells ◽  
Deacetylase Inhibitor

Impact of Hybrid-polar Histone Deacetylase Inhibitor m-Carboxycinnamic Acid bis-Hydroxyamide on Human Pancreatic Adenocarcinoma Cells

2019 ◽  
Vol 19 (6) ◽  
pp. 750-759
Author(s):  
Dinesh Kumar ◽  
Pranjal Sarma ◽  
Manika P. Bhadra ◽  
Anjana D. Tangutur
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Histone Deacetylase ◽  
Pancreatic Adenocarcinoma ◽  
Histone Deacetylase Inhibitor ◽  
Human Pancreatic Adenocarcinoma ◽  
Pancreatic Cancer Cells ◽  
Adenocarcinoma Cells ◽  
Deacetylase Inhibitor

Background: Histone deacetylase inhibitors (HDACIs) have got immense importance as promising drugs for cancer treatment as these inhibitors regulate cellular differentiation, gene expression, cell cycle arrest and apoptosis. The current study investigates the effect of the hybrid-polar HDACI m-carboxycinnamic acid bishydroxyamide (CBHA) on the growth of human pancreatic adenocarcinoma cells, using the cell line MIA PaCa- 2 as an in vitro model. Methods: Following CBHA treatment of the MIA PaCa-2 cells, we characterized the effect of CBHA by in vitro cytotoxicity evaluation, clonogenic assay, cell cycle analysis, immunoblotting for soluble and insoluble fractions of tubulin, immunofluorescence and caspase-3 assay. Results: We observed that the histone deacetylase inhibitor CBHA markedly impaired growth of the pancreatic cancer cells by resulting in dose-dependent G2/M arrest, disruption of microtubule organization, induction of caspase-mediated apoptosis and in vitro suppression of HDAC6. Our study also shows that inhibition of HDAC6 by CBHA induced acetylation of α-tubulin. Conclusion: Together, our findings show that CBHA can be a potential plausible therapeutic that could be exploited for pancreatic cancer therapy.

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