MicroRNA-505 is downregulated in human osteosarcoma and regulates cell proliferation, migration and invasion

Liu, Yu-Jiang; Li, Wei; Chen, Feng; Liu, Jian-Na; Lin, Junxin; Chen, Dexi

doi:10.3892/or.2017.6142

Cited by 26 publications

(37 citation statements)

References 41 publications

(39 reference statements)

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“…However, our understanding of how miRNAs regulate CC development and progression -particularly how they affect CC metastasis -remains limited. Recent studies demonstrate that microRNA-505 (miR-505) is dysregulated in different types of human cancers, including breast cancer, colorectal cancer, prostate cancer, endometrial cancer, bladder cancer, and hepatocellular carcinoma, among others [10][11][12][13][14][15][16][17][18][19][20][21][22]. Furthermore, miR-505 expression levels in plasma [21] and in whole blood [22] could be used as a potential non-invasive biomarker for bladder and pancreatic cancer.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-505-5p functions as a tumor suppressor by targeting cyclin-dependent kinase 5 in cervical cancer

et al. 2019

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MicroRNAs (miRs) are considered to be tumor suppressors or oncogenes as they regulate cell proliferation, migration, invasion, and differentiation. Recently, microRNA-505 (miR-505) has been reported as being involved in the progression of several human cancers. In the present study, we aim to investigate the expression rate and functional role of miR-505-5p in cervical cancer (CC) to determine its significance regarding the disease’s development. The expression of miR-505-5p and cyclin-dependent kinase 5 (CDK5) in specimens of patients with CC and CC cell lines was examined by quantitative real-time PCR (qRT-PCR) and Western Blot. The relationship between miR-505-5p and CDK5 was verified by luciferase reporter assay. Cell counting kit-8 (CCK-8) assay, Scratch wound healing assay and transwell assay were used to detect the roles of miR-505-5p and CDK5 in CC cell functions. Western Blot was utilized to explore the epithelial–mesenchymal transition (EMT) markers. The result showed that in CC tissues and CC cell lines miR-505-5p was down-regulated while CDK5 level was up-regulated. MiR-505-5p was closely correlated with the metastasis-associated clinicopathological features. Overexpression of miR-505-5p inhibited cell viability, cell metastasis and EMT in CC cells. CDK5 was confirmed as a direct target of miR-505-5p and inverse relationship between them was also observed. Overexpression of CDK5 reduces the inhibitory effects of miR-505-5p in CC. Taken together, these results determine that miR-505-5p is a tumor suppressor miRNA which regulates tumor cell proliferation, migration, and invasion via binding to the functional target CDK5 and demonstrates its potential for future use in the treatment of CC.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-505-5p functions as a tumor suppressor by targeting cyclin-dependent kinase 5 in cervical cancer

et al. 2019

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“…MiRNAs are key regulators in the tumorigenesis of OS. Some miRNAs are down-regulated in OS, such as miR-133a, 24 -137, 25 -150, 26 -223, 27 -505, 28 and -564. 29 In consistent with these miRNAs, miR-431-5p was also down-regulated in OS tissues and cells in this study.…”

Section: Discussionmentioning

confidence: 99%

<p>MicroRNA-431-5p Inhibits the Tumorigenesis of Osteosarcoma Through Targeting PANX3</p>

Sun¹,

Fu²,

Wang³

et al. 2020

CMAR

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Purpose This study aimed to evaluate the regulatory role of miR-431-5p on the tumorigenesis of osteosarcoma (OS) and the underlying mechanism involving pannexin 3 ( PANX3 ). Methods qRT-PCR was applied to measure the expression of miR-431-5p in OS tissues and cells. PANX3 and miR-431-5p were overexpressed in U2OS and HOS cells. The cell viability and apoptosis were determined by MTT and FITC/PI double staining assay, respectively. Transwell assay was performed to detect cell migration and invasion. The protein expression of cleave-caspase-3 and MMP-2/-9 was detected by Western blot. The target relationship between miR-431-5p and PANX3 was predicated by ENCORI and identified by DLR assay. The anti-tumor effect of miR-431-5p was further analyzed in a xenograft tumor model in mice. Results MiR-431-5p expression was down-regulated in OS tissues and negatively correlated with lymph node metastasis and TNM stage. Over-expression of miR-431-5p induced cell apoptosis, inhibited cell proliferation, migration and invasion, up-regulated cleave-caspase-3, and down-regulated MMP-2 and -9 in OS cells. Over-expression of miR-431-5p also inhibited the growth of tumor xenografts in mice. In addition, PANX3 was a target of miR-431-5p. Over-expression of PANX3 reversed the anti-tumor effect of miR-431-5p mimics on U2OS and HOS cells. Conclusion Up-regulation of miR-431-5p suppressed the tumorigenesis of OS via targeting PANX3 .

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“…Our results indicated the significant down-regulation of miR-505 in HCC tissues compared with normal controls (data not shown). It has been found that miR-505 suppressed the proliferation, migration and invasion of osteosarcoma cells [15]. The potential tumor suppressive function of miR-505 was also demonstrated in cervical cancer and endometrial cancer [16,17].…”

Section: Introductionmentioning

confidence: 92%

MiR-505 suppressed the growth of hepatocellular carcinoma cells via targeting IGF-1R

et al. 2019

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Hepatocellular carcinoma (HCC) is one of the most common cancers globally. An increasing body of evidence has demonstrated the critical function of microRNAs (miRNAs) in the initiation and progression of human cancers. Here, we showed that miR-505 was down-regulated in HCC tissues and cell lines. Reduced expression of miR-505 was significantly correlated with the worse prognosis of HCC patients. Overexpression of miR-505 suppressed the proliferation, colony formation and induced apoptosis of both HepG2 and Huh7 cells. Further mechanism study uncovered that miR-505 bound the 3′-untranslated region (3′-UTR) of the insulin growth factor receptor (IGF-1R) and inhibited the expression of IGF-1R in HCC cells. The down-regulation of IGF-1R by miR-505 further suppressed the phosphorylation of AKT at the amino acid S473. Consistently, the abundance of glucose transporter (GLUT) 1 (GLUT1) was reduced with the overexpression of miR-505. Down-regulation of GLUT1 by miR-505 consequently attenuated the glucose uptake, lactate production and ATP generation of HCC cells. Collectively, our results demonstrated the tumor suppressive function of miR-505 possibly via inhibiting the glycolysis of HCC cells. These findings suggested miR-505 as an interesting target for designing anti-cancer strategy in HCC.

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MicroRNA-505 is downregulated in human osteosarcoma and regulates cell proliferation, migration and invasion

Cited by 26 publications

References 41 publications

MicroRNA-505-5p functions as a tumor suppressor by targeting cyclin-dependent kinase 5 in cervical cancer

MicroRNA-505-5p functions as a tumor suppressor by targeting cyclin-dependent kinase 5 in cervical cancer

<p>MicroRNA-431-5p Inhibits the Tumorigenesis of Osteosarcoma Through Targeting PANX3</p>

MiR-505 suppressed the growth of hepatocellular carcinoma cells via targeting IGF-1R

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