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Int. J. Mol. Sci. 2018, 19(11), 3546; https://doi.org/10.3390/ijms19113546

NVP-BEZ235 Attenuated Cell Proliferation and Migration in the Squamous Cell Carcinoma of Oral Cavities and p70S6K Inhibition Mimics its Effect

1
Department of Otolaryngology, Chiayi Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Chiayi 61363, Taiwan
2
School of Traditional Chinese Medicine, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan
3
Department of Nursing, I-Shou University, Kaohsiung 82445, Taiwan
4
Department of Otolaryngology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan
5
Division of Hematology-Oncology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan
6
Department of Chinese Medicine, Chiayi Chang Gung Memorial Hospital, Chiayi 61363, Taiwan
7
Division of Hematology and Oncology, Department of Internal Medicine, E-Da Hospital, Kaohsiung 82445, Taiwan
8
School of Medicine, I-Shou University, Kaohsiung 82445, Taiwan
9
Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Tao-Yuan 33302, Taiwan
*
Authors to whom correspondence should be addressed.
Received: 9 October 2018 / Revised: 8 November 2018 / Accepted: 8 November 2018 / Published: 10 November 2018
(This article belongs to the Special Issue mTOR in Human Diseases)
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Abstract

NVP-BEZ235 or BEZ235 is a dual inhibitor of adenosine triphosphate (ATP)-competitive phosphoinositide 3-kinase (PI3K)/mammalian-target-of-rapamycin (mTOR) and is promising for cancer treatment. Because it targets more than one downstream effector, a dual approach is promising for cancer treatment. The aim of this study was to evaluate the efficacy of NVP-BEZ235 in treating oral cavity squamous cell carcinoma (OSCC). Two human OSCC cell lines, SCC-4 and SCC-25, were used in this study. PI3K-AKT signaling, proliferation, and cell migratory and invasion capabilities of OSCC cells were examined. In NVP-BEZ235-treated SCC-4 and SCC-25 cells, the phosphorylation of 70-kDa ribosomal S6 kinase (p70S6K), but not mTOR, decreased within 24 h. NVP-BEZ235 inhibited OSCC-cell proliferation, migration, and invasion possibly by directly deregulating the phosphorylation of p70S6K. The phospho-p70S6K inhibitor mimicked the effects of NVP-BEZ235 for preventing proliferation and weakening the migratory and invasion abilities of SCC-4 and SCC-25 cells. This study further confirmed the effect of NVP-BEZ235 on OSCC cells and provided a new strategy for controlling the proliferation, migration, and invasion of OSCC cells using the phopho-p70S6K inhibitor. View Full-Text
Keywords: oral cavity squamous cell carcinoma (OSCC); NVP-BEZ235; mTOR; p70S6K oral cavity squamous cell carcinoma (OSCC); NVP-BEZ235; mTOR; p70S6K
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Hsu, C.-M.; Lin, P.-M.; Lin, H.-C.; Tsai, Y.-T.; Tsai, M.-S.; Li, S.-H.; Wu, C.-Y.; Yang, Y.-H.; Lin, S.-F.; Yang, M.-Y. NVP-BEZ235 Attenuated Cell Proliferation and Migration in the Squamous Cell Carcinoma of Oral Cavities and p70S6K Inhibition Mimics its Effect. Int. J. Mol. Sci. 2018, 19, 3546.

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