Home|Journals|Articles by Year|Audio Abstracts
 

Original Article

J App Pharm Sci. 2018; 8(9): 130-141


Dendrophthoe pentandra Induced Apoptosis and Cell Cycle Arrest at G1/S in Human Breast Adenocarcinoma Cells, MCF-7 via Up- Regulation of p53

Nik Aina Syazana Nik Zainuddin, Yusmazura Zakaria, Mohd Dasuki Sul’ain.




Abstract

Dendrophthoe pentandra or mistletoe is a semi-parasitic plant with traditional claim of having antiproliferative and anticancer properties. However, the mechanism underlying anticancer activity of this plant remains unclear. This study aims to evaluate the antiproliferative activity of D. pentandra and its mechanism of action in cancer treatment. The extraction of D. pentandra was performed using methanol. The antiproliferative activity of D. pentandra methanol extract using MTT Assay showed inhibition on MCF-7 cell proliferation with IC50 of 10.65 ± 0.49 µg/ml. Hoechst 33258 nuclear staining displayed chromatin condensation, fragmented nuclei and formation of apoptotic bodies upon treatment with IC50 of D. pentandra methanol extract. Mechanism of cell death in D. pentandra methanol extract-treated MCF-7 cells were performed by flow cytometric analysis. The analysis confirmed that D. pentandra methanol extract-treated MCF-7 arrested cell cycle distribution at G1/S phase and induced apoptosis using AnnexinV/propidium iodide double staining. The mechanism of action was further confirmed by determination of protein involved in apoptosis pathway; Bcl-2, Bax, and p53. The findings suggested that the increased p53 was followed by an increase of pro-apoptotic Bax and decrease of anti-apoptotic Bcl-2 that led to apoptosis. In conclusion, the anticancer effect of D. pentandra methanol extract against MCF-7 cells by induction of apoptotic cell death is a promising approach for breast cancer treatment.

Key words: Dendrophthoe pentandra, apoptosis, MCF-7 cells, flow cytometry analysis






Full-text options


Share this Article


Online Article Submission
• ejmanager.com




ejPort - eJManager.com
Refer & Earn
JournalList
About BiblioMed
License Information
Terms & Conditions
Privacy Policy
Contact Us

The articles in Bibliomed are open access articles licensed under Creative Commons Attribution 4.0 International License (CC BY), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.