Int. J. Mol. Sci. 2013, 14(5), 8801-8817; doi:10.3390/ijms14058801
Article

Caffeic Acid Phenethyl Ester Suppresses Proliferation and Survival of TW2.6 Human Oral Cancer Cells via Inhibition of Akt Signaling

1 Institute of Cellular and System Medicine, National Health Research Institutes, Miaoli 35053, Taiwan 2 Translational Center for Glandular Malignancies, National Health Research Institutes, Miaoli 35053, Taiwan 3 Department of Life Sciences, National Central University, Taoyuan City 32001, Taiwan 4 Institute of Biotechnology, National Tsing Hua University, Hsinchu City 30013, Taiwan 5 Division of Environmental Health and Occupational Medicine, National Health Research Institutes, Miaoli 35053, Taiwan 6 National Center for Toxicological Research, National Health Research Institutes, Miaoli 35053, Taiwan 7 Department of Health Risk Management, China Medical University, Taichung City 40402, Taiwan 8 National Institute of Cancer Research, National Health Research Institutes, Miaoli 35053, Taiwan 9 Graduate Program for Aging, China Medical University, Taichung City 40402, Taiwan 10 Ph.D. Program in Tissue Engineering and Regenerative Medicine, National Chung Hsing University, Taichung City 40227, Taiwan
* Author to whom correspondence should be addressed.
Received: 1 March 2013; in revised form: 2 April 2013 / Accepted: 15 April 2013 / Published: 24 April 2013
(This article belongs to the Section Molecular Diagnostics)
PDF Full-text Download PDF Full-Text [1809 KB, uploaded 24 April 2013 13:34 CEST]
Abstract: Caffeic acid phenethyl ester (CAPE) is a bioactive component extracted from honeybee hive propolis. Our observations indicated that CAPE treatment suppressed cell proliferation and colony formation of TW2.6 human oral squamous cell carcinoma (OSCC) cells dose-dependently. CAPE treatment decreased G1 phase cell population, increased G2/M phase cell population, and induced apoptosis in TW2.6 cells. Treatment with CAPE decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip. Overexpression of Akt1 or Akt2 in TW2.6 cells rescued growth inhibition caused by CAPE treatment. Co-treating TW2.6 cells with CAPE and 5-fluorouracil, a commonly used chemotherapeutic drug for oral cancers, exhibited additive cell proliferation inhibition. Our study suggested that administration of CAPE is a potential adjuvant therapy for patients with OSCC oral cancer.
Keywords: oral cancer; caffeic acid phenethyl ester; TW2.6; cell proliferation; cell cycle; Akt; Akt1; Akt2; phospho-Akt Ser473; phospho-Akt Thr 308; FOXO1; FOXO3a; phospho-FOXO1 Thr24; phospho-FoxO3a Thr32; NF-κB; phospho-NF-κB Ser536; Rb; phospho-Rb Ser807/811; Skp2; cyclin D1; p27; 5-fluorouracil

Article Statistics

Load and display the download statistics.

Citations to this Article

Cite This Article

MDPI and ACS Style

Kuo, Y.-Y.; Lin, H.-P.; Huo, C.; Su, L.-C.; Yang, J.; Hsiao, P.-H.; Chiang, H.-C.; Chung, C.-J.; Wang, H.-D.; Chang, J.-Y.; Chen, Y.-W.; Chuu, C.-P. Caffeic Acid Phenethyl Ester Suppresses Proliferation and Survival of TW2.6 Human Oral Cancer Cells via Inhibition of Akt Signaling. Int. J. Mol. Sci. 2013, 14, 8801-8817.

AMA Style

Kuo Y-Y, Lin H-P, Huo C, Su L-C, Yang J, Hsiao P-H, Chiang H-C, Chung C-J, Wang H-D, Chang J-Y, Chen Y-W, Chuu C-P. Caffeic Acid Phenethyl Ester Suppresses Proliferation and Survival of TW2.6 Human Oral Cancer Cells via Inhibition of Akt Signaling. International Journal of Molecular Sciences. 2013; 14(5):8801-8817.

Chicago/Turabian Style

Kuo, Ying-Yu; Lin, Hui-Ping; Huo, Chieh; Su, Liang-Cheng; Yang, Jonathan; Hsiao, Ping-Hsuan; Chiang, Hung-Che; Chung, Chi-Jung; Wang, Horng-Dar; Chang, Jang-Yang; Chen, Ya-Wen; Chuu, Chih-Pin. 2013. "Caffeic Acid Phenethyl Ester Suppresses Proliferation and Survival of TW2.6 Human Oral Cancer Cells via Inhibition of Akt Signaling." Int. J. Mol. Sci. 14, no. 5: 8801-8817.

Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert