Novel Docosahexaenoic Acid Ester of Phloridzin Inhibits Proliferation and Triggers Apoptosis in an In Vitro Model of Skin Cancer

Authors

Theodora Mantso, Northumbria UniversityFollow
Dimitrios T. Trafalis, University of AthensFollow
Sotiris Botaitis, Democritus University of ThraceFollow
Rodrigo Franco, University of Nebraska-LincolnFollow
Aglaia Pappa, Democritus University of ThraceFollow
H. P. Vasantha Rupasinghe, Dalhousie UniversityFollow
Mihalis I. Panayiotidis, Northumbria UniversityFollow

ORCID IDs

0000-0003-3435-0052

0000-0002-1450-3552

Date of this Version

2018

Citation

Antioxidants 2018, 7, 188

Comments

© 2018 by the authors.

Open access

doi:10.3390/antiox7120188

Abstract

Skin cancer is among the most common cancer types accompanied by rapidly increasing incidence rates, thus making the development of more efficient therapeutic approaches a necessity. Recent studies have revealed the potential role of decosahexaenoic acid ester of phloridzin (PZDHA) in suppressing proliferation of liver, breast, and blood cancer cell lines. In the present study, we investigated the cytotoxic potential of PZDHA in an in vitro model of skin cancer consisting of melanoma (A375), epidermoid carcinoma (A431), and non-tumorigenic (HaCaT) cell lines. Decosahexaenoic acid ester of phloridzin led to increased cytotoxicity in all cell lines as revealed by cell viability assays. However, growth inhibition and induction of both apoptosis and necrosis was more evident in melanoma (A375) and epidermoid carcinoma (A431) cells, whereas non-tumorigenic keratinocytes (HaCaT) appeared to be more resistant as detected by flow cytometry. More specifically, PZDHA-induced cell cycle growth arrest at the G2/M phase in A375 and A431 cells in contrast to HaCaT cells, which were growth arrested at the G0/G1 phase. Elevated intracellular generation of reactive oxygen species ROS was detected in all cell lines. Overall, our findings support the potential of PZDHA as a novel therapeutic means against human skin cancer.