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Evidence-Based Complementary and Alternative Medicine
Volume 2017 (2017), Article ID 6793456, 10 pages
Research Article

Induction of Cell Cycle Arrest and Apoptotic Response of Head and Neck Squamous Carcinoma Cells (Detroit 562) by Caffeic Acid and Caffeic Acid Phenethyl Ester Derivative

1Department of Conservative Dentistry with Endodontics, School of Medicine with the Division of Dentistry, Medical University of Silesia in Katowice, Pl. Akademicki 17, 41-902 Bytom, Poland
2Department of Pathology, School of Pharmacy and Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia in Katowice, ul. Ostrogórska 30, 41-200 Sosnowiec, Poland

Correspondence should be addressed to Arkadiusz Dziedzic

Received 3 October 2016; Accepted 19 December 2016; Published 12 January 2017

Academic Editor: Vassya Bankova

Copyright © 2017 Arkadiusz Dziedzic et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Natural polyphenols have been observed to possess antiproliferative properties. The effects, including apoptotic potential of bioactive phenolic compounds, caffeic acid (CA) and its derivative caffeic acid phenethyl ester (CAPE), on cell proliferation and apoptosis in human head and neck squamous carcinoma cells (HNSCC) line (Detroit 562) were investigated and compared. Cancer cells apoptosis rates and cell cycle arrests were analysed by flow cytometry. Exposure to CA and CAPE was found to result in a dose-dependent decrease in the viability of Detroit 562 cells at different levels. CA/CAPE treatment did significantly affect the viability of Detroit 562 cells (MTT results). CAPE-mediated loss of viability occurred at lower doses and was more pronounced, with the concentrations which inhibit the growth of cells by 50% estimated at 201.43 μM (CA) and 83.25 μM (CAPE). Dead Cell Assay with Annexin V labelling demonstrated that CA and CAPE treatment of Detroit 562 cells resulted in an induction of apoptosis at 50 μM and 100 μM doses. The rise of mainly late apoptosis was observed for 100 μM dose and CA/CAPE treatment did affect the distribution of cells in G0/G1 phase. A combination of different phenolic compounds, potentially with chemotherapeutics, could be considered as an anticancer drug.