Abstract

Studies show that caffeic acid (CA) and caffeic acid phenethyl ester (CAPE) are compounds with potent chemopreventive effects. Breast cancer is a common form of aggressive cancer among women worldwide. This study shows a comparison of CA and CAPE activity on triple-negative human caucasian breast adenocarcinoma line cells (MDA-MB-231). MDA-MB-231 cells were treated by CA and CAPE with doses of from 10 to 100 µM, for periods of 24 h and 48 h. Cytotoxicity MTT tests, apoptosis by Annexin V, and cell cycle with Dead Cell Assays were performed. Cytotoxic activity was greater for CAPE compared to CA (both incubation times, same dosage). IC50 values for CAPE were 27.84 µM (24 h) and 15.83 µM (48 h) and for CA > 10,000 µM (24 h) and > 1000 µM (48 h). Polyphenols induced apoptosis, while CAPE (dose dependently), induced a higher apoptotic effect. CAPE also induced cell cycle arrest in S phase (time and dose dependently), CA did it only for 50 and 100 µM. A dose dependent decline was seen for the G0/G1 phase (CAPE, 48 h), as well as elimination of phase G2/M by 100 µM of CAPE (only mild effect for CA). Comparing CA and CAPE activity on MDA-MB-231, CAPE clearly showed better activity for the same dosages and experiment times.

Highlights

  • Breast cancer is a common cancer and is the leading cause of cancer-related deaths among women worldwide

  • The growth inhibiting effects on a MDA-MB-231 cell line treated with caffeic acid (CA) and caffeic acid phenethyl ester (CAPE) was assayed by MTT cell viability

  • Comparing CAPE cytotoxic activity to CA for the MDA-MB-231 cell line (Figure 1a,c), cell viability values for a dose of 10 μM were similar to CA (97.3%), which indicates low cytotoxic effects during the experiment

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Summary

Introduction

Breast cancer is a common cancer and is the leading cause of cancer-related deaths among women worldwide. Studies have shown that breast cancer is a heterogeneous tumor with varying response to treatments. Radiation therapy is effective in the treatment of breast cancer, but it carries. Molecules 2017, 22, 1554 the risk of normal cell damage and radioresistance of tumor cells. The development of radioresistance leads to cancer recurrence of a more aggressive phenotype in patients [1,2,3,4]. Chemopreventive agents act as cell cycle inhibitors. As a result of activation of check points, cellular stress can lead to cell cycle inhibition. G1/S phase control, prevents replication of damaged

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