MicroRNA-224: as a potential target for miR-based therapy of cancer

Chen, Wei; Fan, Xuemei; Mao, Ling; Zhang, Junying; Li, Jian; Wu, Jianzhong; Tang, Jinhai

doi:10.1007/s13277-015-3883-3

Cited by 22 publications

(19 citation statements)

References 62 publications

(74 reference statements)

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“…To the best of our knowledge, this was the first report that the relative levels of miR-224 in different types of breast cancer tissues were associated inversely with the aggressiveness of breast cancers. Although miR-224 has been shown to promote tumorigenesis of HCC, CRC and gastric cancers [7–9] our data suggest that miR-224 may inhibit the development and progression of breast cancers. Hence, our findings argue that miR-224 may have varying functions in regulating the development and progression of different types of cancers.…”

Section: Discussionmentioning

confidence: 64%

“…Previous studies have shown that miR-224 can bind to the tumor suppressors of TNFα-induced protein 1 (TNFAIP1) and Smad4, Raf kinase inhibitor protein (RKIP), apoptosis inhibitor-5 (API-5), PH domain leucine-rich-repeat protein phosphatase 1 (PHLPP1), and PHLPP2 to promote the survival and proliferation of colorectal cancer (CRC) and hepatocellular carcinoma (HCC), but bind to the TRIB1 to promote apoptosis of prostatic cancer cells [7–11]. Furthermore, miR224 binds to the Smad4 and Homeobox D10 (HOXD10) to promote migration of HCC and CRC [8, 12] while it binds to the TPD52 to inhibit migration of prostatic cancer PCa cells [13].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-224 inhibits proliferation and migration of breast cancer cells by down-regulating Frizzled 5 expression

Liu

Shen

et al. 2016

Oncotarget

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The Wnt/β-catenin signaling is crucial for the proliferation and migration of breast cancer cells. However, the expression of microRNA-224 (miR-224) in the different types of breast cancers and its role in the Wnt/β-catenin signaling and the proliferation and migration of breast cancer cells are poorly understood. In this study, the levels of miR-224 in different types of breast cancer tissues and cell lines were examined by quantitative RT-PCR and the potential targets of miR-224 in the Wnt/β-catenin signaling were investigated. The effects of altered miR-224 expression on the frequency of CD44+CD24− cancer stem-like cells (CSC), proliferation and migration of MCF-7 and MDA-MB-231 cells were examined by flow cytometry, MTT and transwell migration. We found that the levels of miR-224 expression in different types of breast cancer tissues and cell lines were associated inversely with aggressiveness of breast cancers. Enhanced miR-224 expression significantly reduced the fizzled 5-regulated luciferase activity in 293T cells, fizzled 5 expression in MCF-7 and MDA-MB-231 cells, the β-dependent luciferase activity in MCF-7 cells, and the nuclear translocation of β-catenin in MDA-MB-231 cells. miR-224 inhibition significantly increased the percentages of CSC in MCF-7 cells and enhanced proliferation and migration of MCF-7 cells. Enhanced miR-224 expression inhibited proliferation and migration of MDA-MB-231 cells, and the growth of implanted breast cancers in vivo. Induction of frizzled 5 over-expression mitigated the miR-224-mediated inhibition of breast cancer cell proliferation. Collectively, these data indicated that miR-224 down-regulated the Wnt/β-catenin signaling possibly by binding to frizzled 5 and inhibited proliferation and migration of breast cancer cells.

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Section: Discussionmentioning

confidence: 64%

Section: Introductionmentioning

confidence: 99%

MicroRNA-224 inhibits proliferation and migration of breast cancer cells by down-regulating Frizzled 5 expression

Liu

Shen

et al. 2016

Oncotarget

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“…A previous review reported by Chen et al [45] demonstrated that miR-224 may be a potential therapeutic target for malignant tumors via targeting associated genes and pathways. In our study, we conducted a meta-analysis including 16 studies from the literature and two studies from microarrays to quantitatively estimate the prognostic capability of miR-224-5p.…”

Section: Discussionmentioning

confidence: 99%

Potential Targets and Clinical Value of MiR-224-5p in Cancers of the Digestive Tract

Zhang

Huang

Chen

2017

Cell Physiol Biochem

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Background/Aims: MicroRNAs participate in various biological processes in malignant tumors. However, the mechanisms of miR-224-5p in digestive system cancers are not fully understood. A comprehensive investigation of the clinical value and potential targets of miR-224-5p in cancers of the digestive tract is necessary. Methods: Expression profiling data and related-prognostic data of miR-224-5p were acquired from Gene Expression Omnibus, The Cancer Genome Atlas, ArrayExpress, and published literature. The potential target mRNAs of miR-224-5p were predicted using bioinformatics methods and finally annotated using Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Results: MiR-224-5p is up-regulated in digestive system cancers (SMD=0.69, 95% CI: 0.43-0.96, P<0.0001) and exhibits a moderate diagnostic ability (AUC=0.84, 95% CI: 0.80-0.87). Our data also demonstrated that miR-224-5p is statistically significantly correlated with overall survival univariate analysis (HR=1.69, 95% CI: 1.15-2.49, P=0.007) and multivariate analysis (HR=2.39, 95% CI: 1.74-3.30, P<0.0001). In total, 388 potential miR-224-5p target mRNAs were predicted by bioinformatics methods. GO annotation analysis revealed that the top terms of miR-224-5p in biological process, cellular component and molecular function were system development, neuron part, and transcriptional activator activity, RNA polymerase II core promoter proximal region sequence-specific binding, respectively. Moreover, eight pathways were identified in KEGG pathway enrichment analysis. Conclusions: MiR-224-5p is up-regulated and has the potential to become a diagnostic and prognostic biomarker in digestive system cancers. MiR-224-5p might play vital roles in cancers of the digestive tract but the exact molecular mechanisms need further study and verification.

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“…This molecule is also reported as a master regulator of cell cycle progression and its overexpression results in G1/S checkpoint release followed by accelerated cell growth [62]. Recent studies have shown that miR-224 is more highly expressed in not only HCC but also esophageal cancer, non-small cell lung cancer, colorectal cancer, cervical cancer and glioma, and this molecule has a proliferative effect on these cancer cells through direct interactions with various tumor-suppressor genes, such as CAMKK2, ADAM17, Homeobox D 10 and RKIP [63][64][65][66][67][68]. Moreover, the clinical relevance of miR-224 had been reported as an indicator of chemoresistance to cisplatin, methotrexate and R-CHOP, radiation sensitivity and a prognostic factor of sorafenib-treated patients [69][70][71][72][73][74].…”

Section: Discussionmentioning

confidence: 99%

Circulating microRNA profiles in plasma: identification of miR-224 as a novel diagnostic biomarker in hepatocellular carcinoma independent of hepatic function

Okajima¹,

Komatsu²,

Ichikawa³

et al. 2016

European Journal of Cancer

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MicroRNA-224: as a potential target for miR-based therapy of cancer

Cited by 22 publications

References 62 publications

MicroRNA-224 inhibits proliferation and migration of breast cancer cells by down-regulating Frizzled 5 expression

MicroRNA-224 inhibits proliferation and migration of breast cancer cells by down-regulating Frizzled 5 expression

Potential Targets and Clinical Value of MiR-224-5p in Cancers of the Digestive Tract

Circulating microRNA profiles in plasma: identification of miR-224 as a novel diagnostic biomarker in hepatocellular carcinoma independent of hepatic function

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