Endoplasmic reticulum stress-induced apoptotic pathway and mitochondrial dysregulation in HeLa cells treated with dichloromethane extract of Dillenia suffruticosa

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Abstract
Pharmacognosy Magazine,2016,12,45s,s86-s95.
Published:February 2016
Type:Original Article
Authors:
Author(s) affiliations:

Wan Abd Ghani Wan Nor Hafiza1, Latifah Saiful Yazan2, Yin Sim Tor3, Jhi Biau Foo3, Nurdin Armania2, Heshu Sulaiman Rahman4
1 Department of Biomedical Sciences, Faculty of Medicine and Health Science, University Putra Malaysia, 43400 UPM Serdang, Selangor; College of Medical Laboratory Technology, Institute for Medical Research, Jin Pahang, 50588 Kuala Lumpur, Malaysia
2 Department of Biomedical Sciences, Faculty of Medicine and Health Science; Laboratory of Molecular Biomedicine, Institute of Bioscience, University Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
3 Laboratory of Molecular Biomedicine, Institute of Bioscience, University Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
4 Department of Microbiology and Pathology, Faculty of Veterinary Medicine; UPM-MAKNA Cancer Research Laboratory, Institute of Bioscience, University Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia

Abstract:

Ethyl acetate and dichloromethane extract of Dillenia suffruticosa (EADS and DCMDS, respectively) can be a potential anticancer agent. The effects of EADS and DCMDS on the growth of HeLa cervical cancer cells and the expression of apoptotic-related proteins had been investigated in vitro. Cytotoxicity of the extracts toward the cells was determined by 5-diphenyltetrazolium bromide assay, the effects on cell cycle progression and the mode of cell death were analyzed by flow cytometry technique, while the effects on apoptotic-related genes and proteins were evaluated by quantitative real-time polymerase chain reaction, and Western blot and enzyme-linked immunosorbent assay, respectively. Treatment with DCMDS inhibited (P < 0.05) proliferation and induced apoptosis in HeLa cells. The expression of cyclin B1 was downregulated that led to G2/M arrest in the cells after treatment with DCMDA. In summary, DCMDS induced apoptosis in HeLa cells via endoplasmic reticulum stress-induced apoptotic pathway and dysregulation of mitochondria. The data suggest the potential application of DCMDS in the treatment of cervical cancer.

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