Suppression of oral cancer by induction of cell cycle arrest and apoptosis using Juniperus communis extract

Author:

Lee Ching-Chang12,Hsiao Chih-Yen34,Lee Shan-Chih56,Huang Xiao-Fan78,Chang Kai-Fu78,Lee Ming-Shih89,Hsieh Ming-Chang89,Tsai Nu-Man89ORCID

Affiliation:

1. Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung 80284, Taiwan, R.O.C.

2. Department of Medical Laboratory Science and Biotechnology, School of Medicine and Health Sciences, FooYin University, Kaohsiung 83102, Taiwan, R.O.C.

3. Division of Nephrology, Department of Internal Medicine, Chia-Yi Christian Hospital, Chia-Yi 60002, Taiwan, R.O.C.

4. Department of Hospital and Health Care Administration, Chia Nan University of Pharmacy and Science, Tainan 71710, Taiwan, R.O.C.

5. Department of Medical Imaging and Radiological Sciences, Chung Shan Medical University, Taichung 40201, Taiwan, R.O.C.

6. Department of Medical Imaging, Chung Shan Medical University Hospital, Taichung 40201, Taiwan, R.O.C.

7. Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan, R.O.C.

8. Department of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung 40201, Taiwan, R.O.C.

9. Clinical Laboratory, Chung Shan Medical University Hospital, Taichung 40201, Taiwan, R.O.C.

Abstract

Abstract The oral cancer incidence rate is slowly increasing and is now the fifth leading cause of cancer-related death due to its high metastasis and recurrence rate. Juniperus communis is used as a traditional Chinese medicine and has been proven to have anti-cancer activity against neuroblastomas. In the present study, we further investigated the anti-cancer mechanisms of J. communis extract (JCo) on oral cancer and evaluated the synergistic effects of JCo combined with 5-fluorouracil (5-FU). We found that JCo inhibited oral cancer cell growth, and that JCo might be less cytotoxic to normal cells than to cancer cells. After JCo treatment, cell cycle arrest was observed at the G0/G1 phase through modulation of p53/p21 and Rb signaling. JCo also caused an increase in the sub-G1 phase and cell apoptosis via the intrinsic and extrinsic apoptosis pathways. JCo combined with 5-FU presented a synergistic effect to reduce cell viability. In conclusion, JCo inhibited oral cancer cell growth by inducing cell cycle arrest and activating cell apoptosis, and JCo significantly synergized with 5-FU. JCo might have the potential to be an adjuvant and a new therapeutic drug for oral cancer treatment.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry,Biophysics

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