microRNA-194 suppresses osteosarcoma cell proliferation and metastasis in vitro and in vivo by targeting CDH2 and IGF1R

Han, Kang; Zhao, Tengda; Chen, Xiang; Bian, Na; Yang, Tao; Ma, Qiang; Cai, Chengkui; Fan, Qingyu; Zhou, Yong; Ma, Baoan

doi:10.3892/ijo.2014.2571

Cited by 68 publications

(73 citation statements)

References 50 publications

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“…Data from a previous study suggested that OS progression is associated with downregulation of miR-143 expression and that the pro-apoptotic function of miR-143 was suppressed by this downregulation, leading to increased expression of Bcl-2, an important anti-apoptotic molecule involved in cell survival [Zhang et al, 2010]. In addition, miR-194 was also downregulated in OS, and overexpression of exogenous miR-194 in OS cells reduced the levels of insulinlike growth factor I receptor (IGF1R) and N-cadherin, thus inhibiting proliferation, migration, and invasion of OS cells [Han et al, 2014]. In this context, miR-150 expression in OS has not been investigated, and the mechanisms involving miR-150 in OS progression remain unknown.…”

confidence: 99%

MicroRNA-150 Inhibits Cell Invasion and Migration and Is Downregulated in Human Osteosarcoma

Xiao

Chen²,

Wang³

et al. 2015

Cytogenet Genome Res

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miR-150 expression in osteosarcoma (OS) cell lines and human osteoblast cells was detected, and OS cell models were transfected with exogenous miR-150 to investigate its role in cell proliferation, invasion, and apoptosis. Our results showed that miR-150 expression in OS cells (MG63, Saos-2, SOSP-9607, and U2OS) was significantly lower compared to the osteoblast hFOB1.19 cell line (all p < 0.01). The expression level of miR-150 in MG63 cells that were transfected with exogenous miR-150 mimics was markedly upregulated, while the miR-150 expression level in the inhibitor group was significantly downregulated (both p < 0.01). Similar results were also found in SOSP-9607 cells. Importantly, exogenous miR-150 expression stimulated cell apoptosis and inhibited proliferation, invasion, and migration. A luciferase reporter assay displayed that miR-150 also regulated Sp1 expression by targeting its 3′-UTR, and qRT-PCR and Western blotting showed that elevated levels of miR-150 may reduce Sp1 protein expression. The mRNA and protein levels of Sp1 were upregulated after transfection with a Sp1-expression plasmid and partially reversed the inhibitory effects of miR-150 on cell proliferation, invasion, and metastasis in MG63 and SOSP-9607 cells, as well as promoted cell apoptosis. In conclusion, miR-150 inhibits cell proliferation, invasion, and metastasis and stimulates cell apoptosis by regulating the expression of Sp1. Therefore, miR-150 may be a potential clinical target for the treatment of OS patients.

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confidence: 99%

MicroRNA-150 Inhibits Cell Invasion and Migration and Is Downregulated in Human Osteosarcoma

Xiao

Chen²,

Wang³

et al. 2015

Cytogenet Genome Res

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“…Therapeutic strategies for osteosarcoma include wide tumor excision, radiotherapy, and multi-agent chemotherapy, all of which have significantly improved the prognosis of patients with osteosarcoma [29,30]. However, patients with osteosarcoma showed a very poor cure rate, and the majority of patients eventually died from complications related to pulmonary metastases [31].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-144 inhibits the proliferation, apoptosis, invasion, and migration of osteosarcoma cell line F5M2

Cui

Wang

2015

Tumor Biol.

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This study is aimed to investigate the role of microRNA-144 (miR-144) in osteosarcoma cell line F5M2 proliferation, apoptosis, invasion, and metastasis. Between 2007 and 2014, 66 cases of osteosarcoma samples in the corresponding adjacent normal tissue samples were selected from surgical resection or biopsy in the Department of Orthopedics, Shengjing Hospital, China Medical University. MiR-144 levels and Ezrin messenger RNA (mRNA) levels in osteosarcoma and the adjacent bone tissues were detected, and clinical and pathological features were analyzed. Exogenous miR-144 was transfected into human osteosarcoma cell lines at two different concentrations (low and high), and the expression levels of miR-144 and Ezrin protein between highly metastatic osteosarcoma cells and lowly metastatic osteosarcoma cells were compared. Real-time polymerase chain reaction (RT-PCR) and Western blot were used for detecting the expression levels of miR-144 or Ezrin protein, respectively. Cell proliferation was measured by methylthiazol tetrazolium (MTT) assay. Cell invasion and migration was evaluated by Transwell assays. Finally, flow cytometry was employed to determine the cell apoptosis. MiR-144 expression in osteosarcoma tissue was significantly lower than that in the surrounding normal bone tissue (P < 0.001), while Ezrin mRNA expression in osteosarcoma tissue was significantly higher than that in the surrounding normal bone tissue (P < 0.001); correlation analysis showed a significant negative correlation between miR-144 and Ezrin mRNA levels (r = 0.982, P < 0.001). MiR-144 and Ezrin mRNA expressions were significantly related with cell metastasis (P < 0.05) but were not related with other clinical factors such as gender, age, tumor location, tumor size, Enneking staging, and Dahlin's histological classification. The results of RT-PCR showed that the expression level of miR-144 in osteosarcoma cells increased after transfected with exogenous miR-144 mimics, and this increase positively correlated with the transfection concentration of miR-144 mimics. Furthermore, Western blotting revealed a significant and dose-dependent decrease in Ezrin protein levels in F5M2 cells transfected with miR-144. MTT and Transwell assays showed that the invasion and metastasis of F5M2 cells was significantly decreased following exogenous overexpression of miR-144. Our study supports the view that the miR-144 may regulate Ezrin protein expression by inhibiting the invasion and metastasis of osteosarcoma cells.

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“…Emerging studies suggest that miR-194 is considered as a tumour suppressor and its targets were identified in many cells and tissues. For example, Han et al demonstrated that overexpression of miR-194 significantly repressed the proliferation, migration, and invasion of osteosarcoma cells in vitro, as well as tumour growth and pulmonary metastasis in vivo by targeting cadherin-2 (CDH2) and insulin-like growth factor 1 receptor (IGF-1R) [12]. In addition, it has been reported that miR-194 inhibited the EMT of EC cells [14] and gastric cancer cells [18].…”

Section: Discussionmentioning

confidence: 99%

“…A growing number of studies have confirmed that miRNAs are differentially expressed in pneumonia, and many of them have been considered as biomarkers of pneumonia [7][8][9]. Among the miRNAs, miR-194 has been widely studied in various cancer cells, and shows complicated functions in regulating cell differentiation [10], cell migration [11], cell proliferation, apoptosis [12], and invasion [13]. For example, Dong et al suggested that miR-194 inhibited epithelial to mesenchymal transition (EMT) of endometrial cancer (EC) cells by targeting oncogene B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI-1) and inhibition of BMI-1 by miR-194 may have therapeutic potential in suppressing EC metastasis [14].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-194 Regulates Lipopolysaccharide-Induced Cell Viability by Inactivation of Nuclear Factor-κ B Pathway

Xie

Yang

Han

et al. 2017

Cell Physiol Biochem

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Abstract:The present study explored the functional role of microRNA (miR)-194 in lipopolysaccharide (LPS) induced lung cell injury, along with the underlying mechanisms and to reveal the potential role in infantile pneumonia. Human fibroblasts WI38 cells were transfected with miR-194 mimic or miR-194 inhibitor, and the transfection efficiency was confirmed by quantitative realtime polymerase chain reaction (qRT-PCR). Thereafter, the cells were treated with or without LPS, and then cell viability, cell apoptosis and mRNA and protein expressions of key proteins of nuclear factor kappa B (NF-κB) pathway including inhibitor of NF-κB (IκB) α, p-65, and B-cell CLL/lymphoma (Bcl) 3 were analyzed. Results showed that overexpression and suppression of miR-194 was effective. Administration of LPS significantly decreased the cell viability and statistically promoted the percentages of apoptotic cells and increased the mRNA and protein expressions of p-65 and Bcl-3 but downregulated IκBα compared to the control group (P < 0.05 or P < 0.01). LPS in combination with miR-194 suppression further enhanced the effects of LPS on cell viability and cell apoptosis compared to the LPS group (P < 0.05). In contrast, LPS in combination with miR-194 overexpression observably reversed the effects of LPS on cell viability, cell apoptosis and mRNA and protein expressions of the key proteins (P < 0.05 or P < 0.01). In conclusion, miR-194 increases the LPS-induced the inhibition of cell viability and increasing of the cell apoptosis by inhibition of NF-κB pathway in WI38 cells. MiR-194 might be a potential targeted therapy for treatment of infantile pneumonia.

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microRNA-194 suppresses osteosarcoma cell proliferation and metastasis in vitro and in vivo by targeting CDH2 and IGF1R

Cited by 68 publications

References 50 publications

MicroRNA-150 Inhibits Cell Invasion and Migration and Is Downregulated in Human Osteosarcoma

MicroRNA-150 Inhibits Cell Invasion and Migration and Is Downregulated in Human Osteosarcoma

MicroRNA-144 inhibits the proliferation, apoptosis, invasion, and migration of osteosarcoma cell line F5M2

MicroRNA-194 Regulates Lipopolysaccharide-Induced Cell Viability by Inactivation of Nuclear Factor-κ B Pathway

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