Title:Suppression of the Viability and Proliferation of HepG2 Hepatocellular Carcinoma Cell Line by Konjac Glucomannan
VOLUME: 18 ISSUE: 9
Author(s):Sakunie Sawai, Mas Sahidayana Mohktar*, Wan Kamarul Zaman Wan Safwani and Thamil Selvee Ramasamy
Affiliation:Centre for Innovation in Medical Engineering, Department of Biomedical Engineering, Faculty of Engineering, University of Malaya, Kuala Lumpur, Centre for Innovation in Medical Engineering, Department of Biomedical Engineering, Faculty of Engineering, University of Malaya, Kuala Lumpur, Centre for Innovation in Medical Engineering, Department of Biomedical Engineering, Faculty of Engineering, University of Malaya, Kuala Lumpur, Stem Cell Biology Laboratory, Department of Molecular Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur
Keywords:Konjac glucomannan, hepatocellular carcinoma, cytotoxicity, cell viability, apoptosis, cellular proliferation.
Abstract:Background: Konjac Glucomannan (KGM) is a water-soluble dietary fibre extracted from Amorphophallus
konjac K. Koch (Araceae). Konjac fibre has been clinically proven as an effective antioxidant agent in
weight control but its traditionally known tumour suppression property remains to be explored.
Objective: The main objective of this study is to determine the potential anti-proliferative effect of KGM on
cancer and normal human liver cell lines, HepG2 and WRL68, respectively.
Method: HepG2 and WRL68 cells were treated with KGM, D-mannose, KGM-D-mannose and 5-fluorouracil.
The morphological changes in those treated cells were observed. Cytotoxic effect of the treatments on cell viability
and proliferation, and apoptosis genes expression were assessed by cytotoxicity assay, flow cytometry
and RT-PCR analyses.
Results: The results show that KGM treatment resulted in reduced viability of HepG2 cells significantly, in line
with the apoptosis-like morphological changes. Up-regulation of BAX and down-regulation of BCL2 genes as
reflected by high Bax to Bcl 2 ratio suggests that the inhibitory effect of KGM on HepG2 cells most likely via
Bcl2/Bax protein pathway. Despite the effectiveness of standard drug 5-FU in suppressing the viability and
proliferation of HepG2 cells, it however, exhibited no selective inhibition of cancer cells as compared to KGM.
Conclusion: Current findings suggested that KGM is a potential anti-cancer compound/drug entity, which could
be an alternative preventive agent against liver cancer.
