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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 946451, 15 pages
Research Article

Active Component of Antrodia cinnamomea Mycelia Targeting Head and Neck Cancer Initiating Cells through Exaggerated Autophagic Cell Death

1Institute of Oral Biology, National Yang-Ming University, No. 155, Section 2, Li-Nong Street, Taipei 11221, Taiwan
2Department of Biotechnology, Hungkuang University, Taichung, Taiwan
3Grape King Inc., Taoyuan County, Taiwan
4Department of Life Science, Fu-Jen University, New Taipei City, Taiwan
5Department of Oral and Maxillofacial Surgery, Mackay Memorial Hospital, Taipei, Taiwan
6Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
7Graduate Institute of Chinese Medical Science and Institute of Medical Science, China Medical University, No. 91, Hsueh-Shih Road, Taichung 40402, Taiwan
8Institute of Basic Medical Science, China Medical University, Taichung, Taiwan
9Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan
10Cancer Research Center & Genome Research Center, National Yang-Ming University, Taipei, Taiwan
11Department of Dentistry, Taipei Veterans General Hospital, Taipei, Taiwan
12National Yang-Ming University, VGH Genome Research Center, Taipei, Taiwan

Received 20 March 2013; Accepted 8 May 2013

Academic Editor: Yu-Jen Chen

Copyright © 2013 Ching-Wen Chang et al. 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.

Supplementary Material

Supplementary Table 1. Effect of YMGKI-1 Treatment on Cancer Cell Lines

Supplementary Figure S1. YMGKI-1 affected the cell viability of SAS-HN-CICs (1 × 107 cells/well of 6-well plate) but not parental SAS (5 × 105 cells/well of 6-well plate). A, Cells were treated with 0, 10, 25, 35 and 50 μg/ml of YMGKI-1 for 24 hr, afterward, stained with propidium iodide (PI) and then examined by flow cytometry. B, Morphologies of parental SAS and SAS-HN-CICs with YMGKI-1 treatment.

Supplementary Figure S2. YMGKI-1 induced caspases activation of SAS-HN-CICs. A, Crude cell extract proteins of YMGKI-1 treated SAS-HN-CICs were collected, electrophorized and analyzed by immunoblotting against anti-Cleaved PARP, anti-Cleaved Caspas-3 or anti-GAPDH serum as indicated.

Supplementary Figure S3. HN-CICs treated with metformin or rapamycin displayed slight induction cell death. A, Morphologies of SAS-HN-CICs with metformin or rapamycin treatment for 96 hr. B, SAS-HN-CICs were treated with metformin (10 mM) or rapamycin (100 nM) for 96 hr. , afterward, stained with propidium iodide (PI) and then examined by flow cytometry.

Supplementary Figure S4. SAS xenograft-derived cells were treated with 0, 10, 25 and 50 μg/ml of YMGKI-1 for 24 hr, afterward; the ALDH activity of drug treated cells was examined by flow cytometry. The data are means ± SD of triplicate samples from three experiments (***, P < 0.005).

  1. Supplementary Materials