Department of Endocrinology and Metabolism, The Third Hospital of Nanchang, Nanchang Key Laboratory of Diabetes, Nanchang, Jiangxi 330009, P.R. China.
Mol Med Rep. 2017 Nov;16(5):6690-6696. doi: 10.3892/mmr.2017.7420. Epub 2017 Aug 31.
Diabetes mellitus is associated with an increased risk of breast cancer, but the molecular mechanism underlying this association remains unclear. The aim of the present study was to investigate the effect of high glucose and high insulin conditions on MCF‑7 breast cancer cells and to elucidate the molecular mechanisms underlying these effects. High glucose and high insulin conditions resulted in increased viability, proliferation, and invasion in MCF‑7 cells compared with normal glucose and low insulin conditions. Reverse transcription‑quantitative polymerase chain reaction and western blot analyses revealed that insulin receptor substrate 1 (IRS1) was significantly upregulated following high glucose and high insulin treatment compared with normal glucose and low insulin conditions. Furthermore, high glucose and high insulin treatment increased the Ras family of proto‑oncogenes (Ras) and RAF1 proto‑oncogene (Raf‑1) protein expression, and activated the phosphorylation of extracellular signal‑regulated kinase (ERK) 1/2. These findings suggest that high glucose and high insulin conditions promoted the proliferation and invasion of MCF‑7 cells by upregulating IRS1 and activating the Ras/Raf/ERK pathway.
糖尿病与乳腺癌风险增加相关，但这种关联的分子机制尚不清楚。本研究旨在探讨高糖和高胰岛素条件对 MCF-7 乳腺癌细胞的影响，并阐明这些影响的分子机制。与正常葡萄糖和低胰岛素条件相比，高糖和高胰岛素条件导致 MCF-7 细胞的活力、增殖和侵袭增加。逆转录-定量聚合酶链反应和 Western blot 分析显示，与正常葡萄糖和低胰岛素条件相比，高糖和高胰岛素处理后胰岛素受体底物 1（IRS1）显著上调。此外，高糖和高胰岛素处理增加 Ras 家族原癌基因（Ras）和 RAF1 原癌基因（Raf-1）蛋白表达，并激活细胞外信号调节激酶（ERK）1/2 的磷酸化。这些发现表明，高糖和高胰岛素条件通过上调 IRS1 和激活 Ras/Raf/ERK 通路促进 MCF-7 细胞的增殖和侵袭。
