MicroRNA-552 enhances metastatic capacity of colorectal cancer cells by targeting a disintegrin and metalloprotease 28

Wang, Jian; Li, Hai; Wang, Yong; Wang, Yunlong; Yan, Xiurui; Zhang, Dong; Ma, Xiaoqiang; Du, Ye; Liu, Xiaoming; Yang, Yinxue

doi:10.18632/oncotarget.12169

Cited by 42 publications

(40 citation statements)

References 41 publications

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“…However, the role of ADAM28 in colorectal cancer remains controversial [20,22]. Here, we provide evidence to show in our current functional study that ADAM28 appears to also play a pathogenic role in the metabolic syndrome.…”

Section: Discussionsupporting

confidence: 68%

The Metalloproteinase ADAM28 Promotes Metabolic Dysfunction in Mice

Herat

Rudnicka

Okada

et al. 2017

IJMS

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Obesity and diabetes are major causes of morbidity and mortality globally. The current study builds upon our previous association studies highlighting that A Disintegrin And Metalloproteinase 28 (ADAM28) appears to be implicated in the pathogenesis of obesity and type 2 diabetes in humans. Our novel study characterised the expression of ADAM28 in mice with the metabolic syndrome and used molecular inhibition approaches to investigate the functional role of ADAM28 in the pathogenesis of high fat diet-induced obesity. We identified that ADAM28 mRNA and protein expression was markedly increased in the livers of mice with the metabolic syndrome. In addition, noradrenaline, the major neurotransmitter of the sympathetic nervous system, results in elevated Adam28 mRNA expression in human monocytes. Downregulation of ADAM28 with siRNA technology resulted in a lack of weight gain, promotion of insulin sensitivity/glucose tolerance and decreased liver tumour necrosis factor-α (TNF-α) levels in our diet-induced obesity mouse model as well as reduced blood urea nitrogen, alkaline phosphatase and aspartate aminotransferase. In addition, we show that ADAM28 knock-out mice also displayed reduced body weight, elevated high density lipoprotein cholesterol levels, and reductions in blood urea nitrogen, alkaline phosphatase, and aspartate aminotransferase. The results of this study provide important insights into the pathogenic role of the metalloproteinase ADAM28 in the metabolic syndrome and suggests that downregulation of ADAM28 may be a potential therapeutic strategy in the metabolic syndrome.

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Section: Discussionsupporting

confidence: 68%

The Metalloproteinase ADAM28 Promotes Metabolic Dysfunction in Mice

Herat

Rudnicka

Okada

et al. 2017

IJMS

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“…The promotive role of miR‐552 in CRC was confirmed recently by Wang et al. and Cao et al. This paper showed that an understanding of the expression and function of miR‐552 in HCC might help to understand the underlying molecular mechanisms.…”

Section: Discussionsupporting

confidence: 53%

“…1 MicroRNAs (miRNAs) are sequences of small noncoding RNAs of 18-22 nt in length. 6 They manipulate the expression levels of more than 60% of human genes at the posttranscriptional level by binding to the 3′ untranslated regions (3′UTR) of their target messenger RNAs (mRNAs). 7 This repression enables them to participate in cellular events, including proliferation, apoptosis and movement.…”

Section: Introductionmentioning

confidence: 99%

MiR‐552 promotes the proliferation, migration and EMT of hepatocellular carcinoma cells by inhibiting AJAP1 expression

Wen

et al. 2018

J Cellular Molecular Medi

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Our goal was to explore the function of miR‐552 and its potential target AJAP1 in hepatocellular carcinoma (HCC) oncogenesis and progression. In this study, bioinformatics analysis was performed to detect abnormally expressed miRNAs. The relationship between miR‐552 and AJAP1 was validated using luciferase reporter assays. RT‐qPCR and Western blot assays were applied to explore the expression level of miR‐552, AJAP1 and epithelial‐mesenchymal transition (EMT) markers. HCC cell proliferation was examined using CCK8 assays, while migration and invasion were investigated using Transwell assays. Nude mouse tumourigenesis models were established to facilitate observation of HCC progression in vivo. Finally, prognostic analysis was performed to discover how the prognosis of HCC patients correlated with miR‐552 and AJAP1 expression. MiR‐552 overexpression in HCC cells promoted HCC cell migration, invasion and EMT by targeting/suppressing AJAP1. Poorer prognosis appeared in HCC patients with higher miR‐552 expression or lower AJAP1 levels. Our findings suggested that miR‐552 promotes HCC oncogenesis and progression by inhibiting AJAP1 expression.

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“…The relative ratio of the net intensity of each sample normalized by the β‐tubulin internal control was calculated as densitometric arbitrary units (A.U.) that served as an index of relative expression of a protein of interest …”

Section: Methodsmentioning

confidence: 99%

Disparate roles of CXCR3A and CXCR3B in regulating progressive properties of colorectal cancer cells

Rong

Chen

et al. 2018

Molecular Carcinogenesis

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Human C‐X‐C Motif Chemokine Receptor 3A (CXCR3A) and CXCR3B are two splice variants of CXCR3 that is involved in a variety of progressive processes of cancer cells, including proliferation, migration, invasion, and tumorigenicity. However, the molecular mechanisms of CXCR3 in colorectal cancer (CRC) remain incomplete understood. In the present study, a significantly up‐regulated CXCR3 protein was firstly observed in CRC tissues and cell lines in comparison with the paired non‐tumor tissues and normal intestinal epithelial cells, which was positively associated with CRC TNM stages. In contrast, CXCR3B was down‐regulated in CRC tumor tissues compared with that in the corresponding paired paracancerous tissues, and negatively correlated with the TNM stages of cancer. Of interest, the overexpression of CXCR3A enhanced the progressive capacity of cell proliferation, migration, invasion in CRC LOVO and HCT116 cells in vitro, and the tumorigenicity in nude mice in vivo. Conversely, the overexpression of CXCR3B exhibited an opposite phenotype of CXCR3A, with an ability to inhibit the progressive properties in CRC cell lines in vitro and tumorigenesis in vivo. In addition, immunoblotting analysis further demonstrated that an increased expression of CXCR3A inhibited the expression of CXCR3B in CRC cells and NCM460 normal colon epithelial cells; vice verse, an overexpression of CXCR3B suppressed the expression of CXCR3A in these cells. These data imply that an interaction between the CXCR3A and CXCR3B may play an important regulatory role in tumorigenicity of CRC, which warrants for further investigation.

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MicroRNA-552 enhances metastatic capacity of colorectal cancer cells by targeting a disintegrin and metalloprotease 28

Cited by 42 publications

References 41 publications

The Metalloproteinase ADAM28 Promotes Metabolic Dysfunction in Mice

The Metalloproteinase ADAM28 Promotes Metabolic Dysfunction in Mice

MiR‐552 promotes the proliferation, migration and EMT of hepatocellular carcinoma cells by inhibiting AJAP1 expression

Disparate roles of CXCR3A and CXCR3B in regulating progressive properties of colorectal cancer cells

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