MiR-155 promotes proliferation of human breast cancer MCF-7 cells through targeting tumor protein 53-induced nuclear protein 1

Zhang, Chunmei; Zhao, Jing; Deng, Hua-yu

doi:10.1186/1423-0127-20-79

Cited by 101 publications

(77 citation statements)

References 34 publications

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“…27,28 Besides its crucial function in the regulation of immunological reactions, miR-155 is linked to cancer [37][38][39] and apoptosis. MiR-155 up-regulation in MCF-7 cells correlated with impeded tumor suppressor mRNA expression, elevated proliferation and reduced apoptosis, 40 miR-155 inhibition in Jurkat cells diminished viability and induced apoptosis 41 and mice treated with antisense miR-155 showed attenuated tumorigenesis resulting from increased apoptosis and inhibited proliferation. 42 To address our hypothesis that miR-155 expression is linked to apoptosis protection in the macrophage immune response, we analyzed the potential modulation of CASP-3 expression by miRNA-155 in LPS-activated RAW 264.7 cells.…”

Section: Discussionmentioning

confidence: 92%

miR-155 targets Caspase-3 mRNA in activated macrophages

et al. 2015

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To secure the functionality of activated macrophages in the innate immune response, efficient life span control is required. Recognition of bacterial lipopolysaccharides (LPS) by toll-like receptor 4 (TLR4) induces downstream signaling pathways, which merge to induce the expression of cytokine genes and anti-apoptotic genes. MicroRNAs (miRNAs) have emerged as important inflammatory response modulators, but information about their functional impact on apoptosis is scarce. To identify miRNAs differentially expressed in response to LPS, cDNA libraries from untreated and LPSactivated murine macrophages were analyzed by deep sequencing and regulated miRNA expression was verified by Northern blotting and qPCR. Employing TargetScan TM we identified CASPASE-3 (CASP-3) mRNA that encodes a key player in apoptosis as potential target of LPSinduced miR-155. LPS-dependent primary macrophage activation revealed TLR4-mediated enhancement of miR-155 expression and CASP-3 mRNA reduction. Endogenous CASP-3 and cleaved CASP-3 protein declined in LPS-activated macrophages. Accumulation of miR-155 and CASP-3 mRNA in miRNA-induced silencing complexes (miRISC) was demonstrated by ARGONAUTE 2 (AGO2) immunoprecipitation. Importantly, specific antagomir transfection effectively reduced mature miR-155 and resulted in significantly elevated CASP-3 mRNA levels in activated macrophages. In vitro translation assays demonstrated that the target site in the CASP-3 mRNA 3'UTR mediates miR-155-dependent Luciferase reporter mRNA destabilization. Strikingly, Annexin V staining of macrophages transfected with antagomir-155 and stimulated with LPS prior to staurosporine (SSP) treatment implied that LPS-induced miR-155 prevents apoptosis through CASP-3 mRNA down-regulation. In conclusion, we report that miR-155-mediated CASP-3 mRNA destabilization in LPS-activated RAW 264.7 macrophages suppresses apoptosis, as a prerequisite to maintain their crucial function in inflammation.

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Section: Discussionmentioning

confidence: 92%

miR-155 targets Caspase-3 mRNA in activated macrophages

et al. 2015

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“…Accumulating evidences show that miRNAs modulate cell proliferation, apoptosis, invasion, and metastasis in human cancers [7][8][9][10]. The dysregulation of miRNAs has been observed in various types of human malignant tumors, including lymphoma, colorectal cancer, lung cancer, breast cancer, liver cancer and glioblastoma [11][12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

MiR-1224-5p acts as a tumor suppressor by targeting CREB1 in malignant gliomas

Qian

Wang

et al. 2015

Mol Cell Biochem

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The dysregulation of miR-1224-5p has been reported in several human cancers. However, the expression and function of miR-1224-5p in glioma remains unknown. The aim of our study was to investigate the effect of miR-1224-5p on glioma cells and to determine its functional signaling mediators. Using 198 glioma samples within the Chinese Glioma Genome Atlas expression dataset, we demonstrated that miR-1224-5p expression is decreased in high-grade gliomas when compared with low-grade gliomas. Differential miR-1224-5p expression in 50 randomly selected samples was verified by in situ hybridization. The expression of miR-1224-5p was shown to positively correlate with overall survival in 82 glioblastoma patients. Exogenous expression of miR-1224-5p in glioma cells suppressed proliferation and invasion and promoted apoptosis. Target prediction algorithms identified a consensus miR-1224-5p recognition site in the 3'UTR of the cAMP response element-binding protein (CREB1) gene, and this sequence was shown to directly confer miR-1224-5p repression in luciferase reporter assays. Furthermore, exogenous miR-1224-5p expression was shown to down-regulate CREB1, as well as its downstream target genes matrix metalloproteinase-9 and B-cell lymphoma-2. Conversely, over-expression of CREB1 reversed the effect of miR-1224-5p on the proliferation, invasion, and apoptosis of glioma cells. These data indicate that miR-1224-5p may inhibit tumor-associated activity in malignant gliomas by targeting CREB1.

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“…TP53INP1 is a p53 target gene and mediates the roles of p53 in the suppression of cell growth and induction of cell apoptosis, functioning as a tumor suppressor (25). TP53INP1 was reported to be downregulated in diverse types of cancer and the decreased expression of TP53INP1 was shown to contribute to the pathogenesis of cancer (26)(27)(28).…”

Section: Mir-96 Directly Regulates Tp53inp1 Foxo1 and Foxo3a Expressmentioning

confidence: 99%

MicroRNA-96 promotes the proliferation of colorectal cancer cells and targets tumor protein p53 inducible nuclear protein 1, forkhead box protein O1 (FOXO1) and FOXO3a

Gao

Wang

2014

Molecular Medicine Reports

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Abstract. MicroRNAs (miRNAs) are a conserved class of small, endogenous, non protein-coding RNA molecules that are capable of regulating gene expression at post-transcriptional levels and are involved in diverse cellular processes, including cancer pathogenesis. It has previously been reported that miRNA-96 (miR-96) is overexpressed in human colorectal cancer (CRC). However, the underlying mechanism of miR-96 regulation in CRC remains to be elucidated. In the present study, miR-96 was confirmed to be upregulated in CRC tissues by reverse transcription quantitative polymerase chain reaction. MTT assay, colony formation assay and cell cycle analysis revealed that miR-96 overexpression led to increased tumor cell viability, colony formation ability and cell cycle progression. By contrast, inhibition of miR-96 resulted in the suppression of cell proliferation. It was also demonstrated that miR-96 reduced the messenger RNA and protein expression levels of tumor protein p53 inducible nuclear protein 1 (TP53INP1), forkhead box protein O1 (FOXO1) and FOXO3a, which are closely associated with cell proliferation. A luciferase reporter assay indicated that miR-96 inhibited luciferase intensity controlled by the 3'UTRs of TP53INP1, FOXO1 and FOXO3a. In conclusion, the results of the present study demonstrated that miR-96 contributed to CRC cell growth and that TP53INP1, FOXO1 and FOXO3a were direct targets of miR-96, suggesting that miR-96 may have the potential to be used in the development of miRNA-based therapies for CRC patients.

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MiR-155 promotes proliferation of human breast cancer MCF-7 cells through targeting tumor protein 53-induced nuclear protein 1

Cited by 101 publications

References 34 publications

miR-155 targets Caspase-3 mRNA in activated macrophages

miR-155 targets Caspase-3 mRNA in activated macrophages

MiR-1224-5p acts as a tumor suppressor by targeting CREB1 in malignant gliomas

MicroRNA-96 promotes the proliferation of colorectal cancer cells and targets tumor protein p53 inducible nuclear protein 1, forkhead box protein O1 (FOXO1) and FOXO3a

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