Effects of Arbutin on Human Breast Cancer MCF-7 Cell Une

Surgical approach, radiotherapy and chemotherapy have been used in cancer treatment for many years.Adverse effects of current treatment methods and patients' lifestyle adversely affect. Therefore, the stakeholders and scientists of the subject have turned to research alternative methods that may be more natural and have less side effects. In this context, the effects of different plant extracts or natural components are investigated in many types of cancer.In this study, the effect of arbutin on inflammation and oxidative stress mediated apoptosis (programmed cell death) in MCF-7 adenocarcinoma cell line was investigated.The effects of arbutin on estrogen receptors, proliferation and endoplasmic reticulum stress in MCF-7 cells were also investigated. In the present study, cytotoxicity levels of α and β-arbutin in human breast adenocarcinoma (MCF-7) cell line were analyzed by MTT (3- (4,5-dimethyl-thiazolyl) -2,5-diphenyltetrazolium bromide test).It was determined that β-arbutin may be more cytotoxic for MCF-7 cells. For this reason, studies were continued with β-arbutin.In order to determine the effect of arbutin on oxidative stress, inflammation, apoptosis, proliferation and endoplasmic reticulum stress in MCF-7 cells, 4 different experimental groups were formed. Groups are as follows: Group 1: control group, Group 2: LD0 dose of β-arbutin applied group; Group 3: LD10 dose of β-arbutin treated group, Group 4: : LD50 dose of β-arbutin applied group. Total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), tumor necrosis factor alpha (TNF) α, interferon gamma (IFN) γ, Interleukin 1 beta (IL-1β) in cell lysates obtained from experimental groups levels were analyzed.The effects of β-arbutin on apoptosis by Caspase 3 analysis, proliferation by Bcl-2 analysis and endoplasmic reticulum stress by GRP78 analysis in MCF-7 cells were determined by using cDNAs synthesized using total RNAs isolated from experimental groups. In immunohistochemical studies, the effects of arbutin on estrogen receptors and p53 levels in MCF-7 cells were determined. At the end of the analyzes, it was determined that β-arbutin doses applied to MCF-7 cells did not affect oxidative stress and endoplasmic reticulum stress in experimental groups. However, inflammation was induced by increasing proinflammatory stokin levels in cells treated with LD50 of β-arbutin. In MCF-7 cells, β-arbutin increased genotoxicity in LD10 and LD50 doses. As a result of molecular and immunohistochemical analyzes, LD50 dose of β-arbutin stimulated p53 and caspase 3 levels and increased apoptosis in MCF-7 cells. In addition, β-arbutin suppressed estrogen receptors at all doses administered to MCF-7 cells. It can be thought that LD50 dose of beta arbutin in MCF-7 cells increases the activation of apoptotic caspase 3 and decreases the activity of ERs via p53 induced by genotoxic and inflammatory effects. Investigation of how these effects of β-arbutin can contribute to the development of a new perspective in treatment. However, further studies are needed to address the interaction of β-arbutin with the ER signaling pathway and DNA.