Active Component of Antrodia cinnamomea Mycelia Targeting Head and Neck Cancer Initiating Cells through Exaggerated Autophagic Cell Death
Figure 3
YMGKI-1 treatment diminishes stemness properties and enhances differentiation capability in HN-CICs. SAS-HN-CICs were treated with YMGKI-1 at different concentration for 24 hr, then stained with anti-GRP78 (a), anti-CD133 (b), or anti-CK18 (c) antibodies, respectively, and quantitated by flow cytometry. Data are means ± SD of triplicate samples from three experiments (**; ***). Dead cells were excluded by gating on the propidium-iodide- (PI-) positive cell fraction. (d) Crude cell extract proteins of YMGKI-1-treated-SAS-HN-CICs were collected, electrophores, and analyzed by immunoblotting against anti-Oct-4, anti-Nanog, anti-Notch2, anti-GRP78, anti-E-cadherin, or anti-GAPDH antibodies as indicated. The immunoactive signal of GAPDH protein of different crude cell extracts was referred as loading control. The same concentration (0.03%) of vehicle (DMSO) was added to all control groups.
