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Molecules 2017, 22(3), 472; doi:10.3390/molecules22030472

A Flavone Constituent from Myoporum bontioides Induces M-Phase Cell Cycle Arrest of MCF-7 Breast Cancer Cells

1
Department of Marine Technology and Resources, National Sun-Yat-sen University, Kaohisung 804, Taiwan
2
Division of Hematology and Oncology, Department of Internal Medicine, China Medical University Hospital, Taichung 404, Taiwan
3
College of Medicine, China Medical University, Taichung 404, Taiwan
4
Department of Pharmacy, Kinmen Hospital, Kinmen 891, Taiwan
5
Cancer Center, China Medical University Hospital, Taichung 404, Taiwan
6
School of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, Taiwan
7
School of Pharmacy, Taipei Medical University, Taipei 110, Taiwan
8
Department of Fragrance and Cosmetic Science, College of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, Taiwan
*
Author to whom correspondence should be addressed.
Academic Editor: Derek J. McPhee
Received: 29 December 2016 / Revised: 4 March 2017 / Accepted: 13 March 2017 / Published: 15 March 2017
(This article belongs to the Section Natural Products)
View Full-Text   |   Download PDF [3114 KB, uploaded 19 March 2017]   |  

Abstract

Abstract: Myoporum bontioides is a traditional medicinal plant in Asia with various biological activities, including anti-inflammatory and anti-bacterial characteristics. To identify the bioactive constituents from M. bontioides, a newly-identified flavone, 3,4′-dimethoxy-3′,5,7-trihydroxyflavone (compound 1), along with eight known compounds, were investigated in human MCF-7 breast cancer, SCC4 oral cancer, and THP-1 monocytic leukemia cells. Among these compounds, compound 1 exhibited the strongest antiproliferative activity with half-maximal inhibitory concentration (IC50) values ranging from 3.3 μM (MCF-7) to 8.6 μM (SCC4). Flow cytometric analysis indicated that compound 1 induced G2/M cell cycle arrest in MCF-7 cells. Mechanistic evidence suggests that the G2/M arrest could be attributable to compound 1’s modulatory effects on the phosphorylation and expression of numerous key signaling effectors, including cell division cycle 2 (CDC2), CDC25C, and p53. Notably, compound 1 downregulated the expression of histone deacetylase 2 (HDAC2) and HDAC4, leading to increased histone H3 acetylation and p21 upregulation. Together, these findings suggest the translational potential of compound 1 as a breast cancer treatment. View Full-Text
Keywords: Myoporum bontioides; Myoporaceae; flavone; cell cycle arrest; breast cancer Myoporum bontioides; Myoporaceae; flavone; cell cycle arrest; breast cancer
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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    Description: The 1H and 13C-NMR, HMQC, HMBC, and NOESY plots of compound 1.

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MDPI and ACS Style

Weng, J.-R.; Bai, L.-Y.; Lin, W.-Y.; Chiu, C.-F.; Chen, Y.-C.; Chao, S.-W.; Feng, C.-H. A Flavone Constituent from Myoporum bontioides Induces M-Phase Cell Cycle Arrest of MCF-7 Breast Cancer Cells. Molecules 2017, 22, 472.

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