microRNA-99a inhibits cell proliferation, colony formation ability, migration and invasion by targeting fibroblast growth factor receptor 3 in prostate cancer

Wu, Donghai; Zhou, Yifei; Pan, Huixing; Qü, Ping; Zhou, Jian

doi:10.3892/mmr.2014.2792

Cited by 15 publications

(10 citation statements)

References 36 publications

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“…Interestingly, this protein has been shown through high-affinity protein/protein interactions to inhibit MMP-9 activity (35). Mmp-11, also significantly elevated in the p1158/59 treated animals (Table 1), is highly associated with cell migration and invasion (36). …”

Section: Resultsmentioning

confidence: 99%

A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis

Lindsey

Iyer

Zamilpa

et al. 2015

Journal of the American College of Cardiology

143

118

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Background Proteolytically-released extracellular matrix (ECM) fragments, matricryptins, are biologically active and play important roles in wound healing. Following myocardial infarction (MI), collagen I, a major component of cardiac ECM, is cleaved by matrix metalloproteinases (MMPs). Objectives We identified novel collagen-derived matricryptins generated post-MI that mediate remodeling of the left ventricle (LV). Results In situ, MMP-2 and -9 generate a collagen Iα1 C-1158/59 fragment, and MMP-9 can further degrade it. The C-1158/59 fragment was identified post-MI both in human plasma and mouse LV at levels that inversely correlated to MMP-9 levels. We synthesized a peptide beginning at the cleavage site (p1158/59, amino acids 1159 to 1173) to investigate its biological functions. In vitro, p1158/59 stimulated fibroblast wound healing and robustly promoted angiogenesis. In vivo, early post-MI treatment with p1158/59 reduced LV dilation at day 7 post-MI by preserving LV structure (p < 0.05 versus control). The p1158/59 stimulated both in vitro and in vivo wound healing by enhancing basement membrane proteins, granulation tissue components, and angiogenic factors. Conclusions Collagen Iα1 matricryptin p1158/59 facilitates LV remodeling post-MI by regulating scar formation through targeted ECM generation and stimulation of angiogenesis.

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Section: Resultsmentioning

confidence: 99%

A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis

Lindsey

Iyer

Zamilpa

et al. 2015

Journal of the American College of Cardiology

143

118

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“…Each of these microRNA genes has been observed to be upregulated in a diverse set of malignancies. MIR99A has been shown to repress metastasis in several cancer types and to inhibit MTOR pathway signaling (Wu et al 2015; Yu et al 2015; Yang et al 2014; Warth et al 2015). MIRLET7c has been reported to suppress cell growth, migration and invasion in nasopharyngeal and non-small cell lung cancer (Liu et al 2014; Zhao et al 2014).…”

Section: Non-coding Gene Content Of Hsa21qmentioning

confidence: 99%

Mouse models of Down syndrome: gene content and consequences

2016

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Down syndrome (DS), trisomy of human chromosome 21 (Hsa21), is challenging to model in mice. Not only is it a contiguous gene syndrome spanning 35 Mb of the long arm of Hsa21, but orthologs of Hsa21 genes map to segments of three mouse chromosomes, Mmu16, Mmu17 and Mmu10. The Ts65Dn was the first viable segmental trisomy mouse model for DS; it is a partial trisomy currently popular in preclinical evaluations of drugs for cognition in DS. Limitations of the Ts65Dn are: (i) it is trisomic for 125 human protein coding orthologs, but only 90 of these are Hsa21 orthologs; and (ii) it lacks trisomy for ~75 Hsa21 orthologs. In recent years, several additional mouse models of DS have been generated, each trisomic for a different subset of Hsa21 genes or their orthologs. To best exploit these models and interpret results obtained with them, prior to proposing clinical trials, an understanding of their trisomic gene content, relative to full trisomy 21, is necessary. Here we first review functional information on Hsa21 protein coding genes and the more recent annotation of a large number of functional RNA genes. We then discuss the conservation and genomic distribution of Hsa21 orthologs in the mouse genome and the distribution of mouse-specific genes. Lastly, we consider the strengths and weaknesses of mouse models of DS based on the number and nature of the Hsa21 orthologs that are, and are not, trisomic in each, and discuss their validity for use in preclinical evaluations of drug responses.

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“…The transfected cells were harvested 48 h post-transfection by using 0.2% trypsin/EDTA solution (Gibco) and washed with fetal bovine serum (FBS)-free RPMI-1640 medium. A total of 5x10 4 transfected cells in FBS-free RPMI-1640 medium were added to the upper chamber. RPMI-1640 medium supplemented with 10% FBS was then added to the lower chamber to serve as chemoattractant.…”

Section: Reverse Transcription-quantitative Polymerase Chain Reactionmentioning

confidence: 99%

“…In recent years, the incidence and mortality of PCa in China have gradually increased with progressing economy (3). Despite the unclear aetiology of this malignancy, both hereditary and environmental components have been demonstrated to participate in prostate carcinogenesis, where age, race and family history are the only well-established risk factors (4,5). Over the past decades, considerable advances have been achieved in the diagnosis and treatment of PCa.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑136 inhibits prostate cancer cell proliferation and invasion by directly targeting mitogen‑activated protein kinase kinase 4

et al. 2018

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Prostate cancer (PCa) is the second most common type of cancer and the 6th leading cause of cancer‑associated mortality worldwide. Accumulated evidence suggests that PCa initiation and progression are controlled by microRNAs (miRNAs). Therefore, investigating PCa‑associated miRNAs may provide novel biomarkers for the diagnosis and treatment of patients with PCa. In the present study it was demonstrated that miRNA‑136 (miR‑136) expression was significantly downregulated in PCa tissues and cell lines. The resumption of miR‑136 expression suppressed cell proliferation and invasion in PCa cells. Bioinformatics analysis predicted that mitogen‑activated protein kinase kinase 4 (MAP2K4) was a direct target of miR‑136. This prediction was experimentally confirmed by a luciferase reporter assay, RT‑qPCR and western blot analysis. MAP2K4 was highly expressed in PCa tissues and inversely correlated with the miR‑136 expression level. Additionally, the restoration of MAP2K4 expression significantly blocked the inhibitory effects of miR‑136 on cell proliferation and invasion in PCa cells. Therefore, miR‑136 may suppress the proliferation and invasion of PCa cells by targeting MAP2K4 and may be a novel candidate target for cancer therapy against PCa.

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microRNA-99a inhibits cell proliferation, colony formation ability, migration and invasion by targeting fibroblast growth factor receptor 3 in prostate cancer

Cited by 15 publications

References 36 publications

A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis

A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis

Mouse models of Down syndrome: gene content and consequences

MicroRNA‑136 inhibits prostate cancer cell proliferation and invasion by directly targeting mitogen‑activated protein kinase kinase 4

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