The autophagic inhibition oral squamous cell carcinoma cancer growth of 16-hydroxy-cleroda-3,14-dine-15,16-olide
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Ming-Fang Cheng1,2, Shian-Ren Lin3, Fong-Jen Tseng3,4, Yi-Chao Huang5, May-Jywan Tsai6, Yaw-Syan Fu7 and Ching-Feng Weng3
1Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
2Division of Histological and Clinical Pathology, Hualian Armed Forces General Hospital, Hualien, Taiwan
3Department of Life Science and Institute of Biotechnology, National Dong Hwa University, Hualien, Taiwan
4Department of Orthopedics, Hualien Armed Forces General Hospital, Hualien, Taiwan
5Taoyuan Armed Forces General Hospital, Taoyuan, Taiwan
6Neural Regeneration Laboratory, Department of Neurosurgery, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan
7Department of Biomedical Science and Environmental Biology, Kaohsiung Medical University, Kaohsiung, Taiwan
Ching-Feng Weng, email: [email protected]
Keywords: autophagy, 16-hydroxy-cleroda-3,14-dine-15,16-olide, long-leaf polyalthia, oral squamous carcinoma, xenograft tumor
Received: March 04, 2017 Accepted: May 09, 2017 Published: July 04, 2017
16-hydroxycleroda-3, 13-dine-15, 16-olide (HCD) isolated from Polyalthia longifolia possesses numerous biological activities. Previous studies have reported that HCD can block phosphorylation activity of cancer cells to inhibit tumor cell growth, but the anti-tumor activity in oral squamous cell carcinoma is unrevealed. This study investigates the inhibiting effect of HCD on human OSCC cell growth; thereby, developing a new oral cancer drug. In in vitro cultured human OSCC cells (OECM1 and SAS) were employed to test the inhibitory growth of HCD via cell cytotoxic effect using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, Western blotting, and further determining of the inhibitory efficacy of tumor growth by a xenograft tumor on BALB/c male nude mice (in vivo test). Under various concentrations of HCD and time course treatments were shown to effectively cause cell death and cell-cycle arrest in OECM1 and SAS cells, which was confirmed via a clinical drug (cisplatin) as a positive control. In addition, HCD induced the autophagic cell death in OECM1 and SAS cells by LC3-mediated LC3-I/LC3-II/p62 pathway at the in vitro level. An in vivo assay indicated that HCD could treat oral cancer by deferring tumor growth. These findings provide a favorable assessment for further elucidating the role of HCD that targets autophagic cell death pathways as a potential agent for cancer therapy.
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