Abstract

Objective:Using nutraceuticals in cancer therapy is a strategy contributing with other approaches to promote apoptosis in cancer cells. Myricetin is a polyphenol flavonoid that forms main ingredients of various type of foods and beverages. The inducing properties of myricetin in apoptosis is reported by several investigations. The present study aimed to assess apoptotic effects of myricetin on T47D breast cancer cells and to evaluate part of the mechanisms of action. Materials and Methods: T47D breast cancer cells were assigned into five groups: control (cells in normal condition), myricetin (cells treated with myricetin IC50 concentration) in two different incubation times (24, 48 and 72 hours). MTT assay, annexin v assay, flow cytometry, caspase-3 assay and Real-time PCR were used to evaluate apoptosis in breast cancer cells. Results:The expression rate of apoptotic genes caspase-3, caspase-8, caspase-9, the ratio of BAX /Bcl-2 as well as the expression of P53, BRCA1, GADD45 genes were increased significantly after treatment of T47D breast cancer cells with myricetin. Annexin v assay confirmed significant expression of annexin as were displyed by flow cytometry. Conclusion:Myricetin enhances apoptosis in T47D breast cancer cells by evoking both extrinsic and intrinsic apoptotic pathways. myricetin may practices its apoptotic properties on T47D cells through inducing BRCA1- GADD45 pathway.

Highlights

  • Breast cancer is the second causes of death and the most prevalent cancer among women in the world (Boulton, 2006)

  • Materials and Methods: T47D breast cancer cells were assigned into five groups: control, myricetin in two different incubation times (24, 48 and 72 hours)

  • MTT assay and IC50 dose response curve Approaching the results of MTT assay, a dose response curve for myricetin was depicted and 46 μM considered as IC50 (Figure 1)

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Summary

Introduction

Breast cancer is the second causes of death and the most prevalent cancer among women in the world (Boulton, 2006). Studies have shown that flavonoids have various biological functions, such as changing epigenetics (Dashwood, 2007; Gilbert and Liu, 2010) They can increase the expression level of tumor suppressor mRNAs and induces apoptosis in the cell (Harkin et al, 1999; Gilbert and Liu, 2010). The role of mutations of tumor suppressor genes in onset and progression of many type of cancers is well recognized (Lee, 1989). Mutation in many tumor suppressor genes such as TP53, BRCA1, and BRCA2 involve in the onset and progression of breast cancer (Rice et al, 2000; Dagdemir et al, 2013)

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