Department of Chest Surgery, The First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710061, China; Department of Tumor, SenGong Hospital of Shaanxi, Xi'an 710300, China.
Biochem Biophys Res Commun. 2013 Nov 8;441(1):139-43. doi: 10.1016/j.bbrc.2013.10.025. Epub 2013 Oct 12.
An increasing number of studies have shown that miRNAs are commonly deregulated in human malignancies, but little is known about the function of miRNA-205 (miR-205) in human breast cancer. The present study investigated the influence of miR-205 on breast cancer malignancy.
The expression level of miR-205 in the MCF7 breast cancer cell line was determined by quantitative (q)RT-PCR. We then analyzed the expression of miR-205 in breast cancer and paired non-tumor tissues. Finally, the roles of miR-205 in regulating tumor proliferation, apoptosis, migration, and target gene expression were studied by MTT assay, flow cytometry, qRT-PCR, Western blotting and luciferase assay.
miR-205 was downregulated in breast cancer cells or tissues compared with normal breast cell lines or non-tumor tissues. Overexpression of miR-205 reduced the growth and colony-formation capacity of MCF7 cells by inducing apoptosis. Overexpression of miR-205 inhibited MCF7 cell migration and invasiveness. By bioinformation analysis, miR-205 was predicted to bind to the 3' untranslated regions of human epidermal growth factor receptor (HER)3 mRNA, and upregulation of miR-205 reduced HER3 protein expression.
miR-205 is a tumor suppressor in human breast cancer by post-transcriptional inhibition of HER3 expression.
越来越多的研究表明，miRNAs 在人类恶性肿瘤中普遍失调，但miRNA-205（miR-205）在人类乳腺癌中的功能知之甚少。本研究探讨了 miR-205 对乳腺癌恶性程度的影响。
通过定量（q）RT-PCR 测定 MCF7 乳腺癌细胞系中 miR-205 的表达水平。然后分析了 miR-205 在乳腺癌和配对非肿瘤组织中的表达。最后，通过 MTT 测定、流式细胞术、qRT-PCR、Western blot 和荧光素酶测定研究了 miR-205 调节肿瘤增殖、凋亡、迁移和靶基因表达的作用。
与正常乳腺细胞系或非肿瘤组织相比，乳腺癌细胞或组织中 miR-205 下调。miR-205 的过表达通过诱导细胞凋亡降低 MCF7 细胞的生长和集落形成能力。miR-205 的过表达抑制 MCF7 细胞迁移和侵袭。通过生物信息学分析，预测 miR-205 结合人表皮生长因子受体（HER）3 mRNA 的 3'非翻译区，上调 miR-205 降低 HER3 蛋白表达。
miR-205 通过对 HER3 表达的转录后抑制，成为人类乳腺癌中的肿瘤抑制因子。
