β-Eudesmol induces the expression of apoptosis pathway proteins in cholangiocarcinoma cell lines

Background: Cholangiocarcinoma (CCA) is a neglected disease prevalent in developing countries with high burden and mortality rate, and there is no effective treatment. We aimed to investigate β-eudesmol molecular target of action in human CCA cell lines using the selected key molecules of apoptotic...

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Bibliographic Details
Main Authors: Chisato Narahara, Teerachat Saeheng, Wanna Chaijaroenkul, Shyam Prakash Dumre, Kesara Na-Bangchang, Juntra Karbwang
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2020-01-01
Series:Journal of Research in Medical Sciences
Subjects:
Online Access:http://www.jmsjournal.net/article.asp?issn=1735-1995;year=2020;volume=25;issue=1;spage=7;epage=7;aulast=Narahara
Description
Summary:Background: Cholangiocarcinoma (CCA) is a neglected disease prevalent in developing countries with high burden and mortality rate, and there is no effective treatment. We aimed to investigate β-eudesmol molecular target of action in human CCA cell lines using the selected key molecules of apoptotic pathways. Materials and Methods: Two CCA cell lines (HuH28 and HuCCT1) were assessed at different time points after β-eudesmol treatment for mRNA and protein expression profiles of caspase-3, -8, -9, p53, p21, Bcl-2, and Bax by real-time polymerase chain reaction and western blot, respectively. Results: β-eudesmol induced expressions of p21 and p53 in mRNA/protein level in HuH28 and HuCCT1 cells. These CCA cells also expressed caspase-3, -8, -9 and bax (mRNA and/or protein level) among others after β-eudesmol treatment indicating its role in both intrinsic and extrinsic caspase-dependent apoptotic pathways. Conclusion: The study demonstrated that β-eudesmol induced the expression of apoptosis pathway proteins, suggesting its potential role in promoting the caspase-dependent apoptotic pathway, and induction of the cell cycle arrest in CCA cell lines. β-eudesmol can be considered as a potential compound for further investigation as an anti-CCA agent.
ISSN:1735-1995
1735-7136