Abstract
BackgroundMiR-155 has emerged as an “oncomiR”, which is the most significantly up-regulated miRNA in breast cancer. However, the mechanisms of miR-155 functions as an oncomiR are mainly unknown. In this study, the aims were to investigate the effects of miR-155 on cell proliferation, cell cycle, and cell apoptosis of ERalpha (+) breast cancer cells and to verify whether TP53INP1 (tumor protein 53-induced nuclear protein 1) is a target of miR-155, and tried to explore the mechanisms of miR-155 in this process.ResultsThe expression of miR-155 is significantly higher in MCF-7 cells compared with MDA-MB-231 cells. Ectopic expression of TP53INP1 inhibits growth of MCF-7 cells by inducing cell apoptosis and inhibiting cell cycle progression. Overexpression of miR-155 increases cell proliferation and suppress cell apoptosis, whereas abrogating expression of miR-155 suppress cell proliferation and promotes cell apoptosis of MCF-7 cells. In addition, miR-155 negatively regulates TP53INP1 mRNA expression and the protein expression of TP53INP1, cleaved-caspase-3, -8, -9, and p21, and luciferase reporter reveals that TP53INP1 is targeted by miR-155.ConclusionsTP53INP1 is the direct target of miR-155. MiR-155, which is overexpressed in MCF-7 cells, contributes to proliferation of MCF-7 cells possibly through down-regulating target TP53INP1.
Highlights
MiR-155 has emerged as an “oncomiR”, which is the most significantly up-regulated miRNA in breast cancer
We found that miR-155 expression was significantly higher in MCF-7 cells with ERalpha (+) compared with MDA-MB-231 cells with ERalpha (−) using real-time PCR analysis
Ectopic expression of TP53INP1 inhibits growth of MCF-7 cells by inducing cell apoptosis and inhibiting cell cycle progression MCF-7 cells were transfected with TP53INP1 overexpression plasmid or control plasmid, and CCK8 assay showed there was a significant reduction in the growth of TP53INP1-expressing cells compared to those transfected with the control plasmid (Figure 2A)
Summary
MiR-155 has emerged as an “oncomiR”, which is the most significantly up-regulated miRNA in breast cancer. MiR-155 represents a typical multifunctional miRNA, which is overexpressed in a variety of human solid tumors such as breast cancer [9,10,11,12], lung cancer [13,14], thyroid tumor [15], pancreatic cancer [16,17,18,19] These recent clinical pathologic data indicate that miR-155 plays a crucial role in tumor development and tumor diagnosis and prognosis. The available experimental evidences indicate that miR-155 promotes some tumors growth, invasion, and metastasis through inhibits downstream targets such as SHIP1 [20], C/EBPbeta [21], and SOCS1 [11]. All these lines of evidence demonstrate that miR-155 functions as an oncomiR in human cancer
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