Effects of leptin on the viability of MCF-7 and T47D cells at different glucose concentrations

Year 2020, Volume: 37 Issue: 4, 119 - 125, 11.09.2020

Pınar Demirel , Soner Dogan , Ümit Özorhan , Bilge Güvenç Tuna , Todd Schuster , Margot Cleary

Abstract

Obesity is associated with increased risk of breast cancer. Leptin is a well-known factor involved in obesity and its serum levels are increased in breast cancer. Hyperglycemia is another significant risk factor for breast cancer. Consistently, high glucose induces proliferation and invasion of breast cancer cells and in vivo calorie restriction reduces tumorigenesis in rodent models. The aim of this study was to investigate the effect of leptin on the viability and mode of cell death in breast cancer cells incubated in different glucose concentrations to represent caloric restriction. For this purpose, MCF-7 and T47D breast cancer cells incubated in different glucose concentrations for a total of 72 hours were treated with or without leptin either for one hour or 24 hours and the ratio of apoptotic, necrotic and alive cells were analyzed by flow cytometry. Our data revealed that glucose incubation significantly decreased apoptosis and necrosis, while increasing viability in both cell lines in a dose dependent manner. One-hour leptin treatment significantly decreased viability, and increased apoptosis but did not significantly affect necrosis in T47D cells incubated in 2.5 mM glucose. In MCF-7 cells, one-hour leptin incubation significantly increased necrosis but its effects on apoptosis and viability were not significant. In conclusion, glucose induces cell death by apoptosis and necrosis in T47D and MCF-7 cells, respectively in a dose dependent manner. One-hour leptin treatment reverses the effect of low glucose incubation on apoptosis of T47D and necrosis of MCF-7 cells. Moreover, the effect of one-hour leptin treatment on apoptosis or necrosis is significantly higher than that of 24-hour leptin treatment.

Keywords

Leptin, Glucose, MCF-7, T47D, Cancer, Breast Cancer, Cell Viability

Supporting Institution

NIH (National Institute of Health) and The Breast Cancer Research Foundation and The Hormel Foundation, Minnesota.

Project Number

CA101858 and CA157012 (MPC) and The Breast Cancer Research Foundation and The Hormel Foundation, Minnesota.

Thanks

This work was supported by grants NIH-CA101858, CA157012 (MPC) and The Breast Cancer Research Foundation and The Hormel Foundation, Minnesota. The authors thank summer intern undergraduate student, Swetha S. Ramanan, for helping us maintaining the cell culture.

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