Abstract
Statins, a class of hyperlipidemic drugs, are widely used cholesterol lowering drugs that selectively inhibit 3-hydroxy-3-methylglutaryl CoA reductase, which is the rate-limiting enzyme in cholesterol biosynthesis, leading to decreasing of cholesterol biosynthesis. Statins exert anti-tumoral effects on various cancer, including breast cancer. However, the molecular mechanisms for the actions were not fully elucidated. The purpose of this study was to elucidate the effects of statins on proliferation and apoptosis in the ER-negative breast cancer cell line MDA-MB-231. Our results showed that simvastatin increased the expression of miR-140-5p in a dose dependent manner via activating transcription factor NRF1, reduced cell proliferation and induced apoptosis, and we also found that SLC2A1 was a new target of miR-140-5p. In conclusion, data in this study shed light on the potential anti-tumoral effects of simvastatin in breast cancer and presents a highly promising therapeutic option, using drug and miRNA for combined treating cancers.
Highlights
Breast cancer is the most common cancer among women all over the world [1,2]
Our results showed that simvastatin increased the expression of miR-140-5p in a dose dependent manner via activating transcription factor nuclear respiratory factor 1 (NRF1), reduced cell proliferation and induced apoptosis, and we found that solute carrier family 2 member 1 (SLC2A1) was a new target of miR-140-5p
The results showed that both simvastatin and miR-140-5p alone increase cell death, and combination of miR-140-5p transfection with simvastatin led to a significantly increase of cell death compared with the them alone (Fig. 7A). miR-140-5p or negative control designed as a short hairpin RNA was brought into MDA-MB-231 cells by a lentivirus vector, which has an EGFP Reporter
Summary
Breast cancer is the most common cancer among women all over the world [1,2]. Approximately 15% of breast tumors are triple negative breast cancers (TNBC). TNBC have the poorest survival outcome of all breast cancer subtypes [3]. This is due to its high propensity for metastatic progression and resistance to endocrine therapy [4, 5]. Simvastatin exhibits antitumor activity in a variety of cancers including lung cancer and gastric cancer [14,15,16]. Despite this knowledge, in order to improve and increase the www.aging-us.com therapeutic effect of simvastatin on cancer, a more complete understanding of simvastatin induced apoptosis is needed
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