MicroRNA cloning and sequencing in osteosarcoma cell lines: differential role of miR-93

Montanini, Luisa; Lasagna, Lisa; Barili, Valeria; Jonstrup, Søren Peter; Murgia, Alba; Pazzaglia, Laura; Conti, Amalia; Novello, Chiara; Kjems, Jørgen; Perris, Roberto; Benassi, Maria Serena

doi:10.1007/s13402-011-0059-z

Cited by 43 publications

(39 citation statements)

References 47 publications

(49 reference statements)

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“…miR-93 is one of the miRNAs that are aberrantly expressed in tumoral tissues compared with nontumoral tissues. It has been recognized as an oncogenic miRNA that is upregulated in several types of cancer, including smallcell lung cancer [22], osteosarcoma [23], laryngeal cancer [24], hepatocellular carcinoma [13], gastric cancer [14], and ovarian cancer [25]. However, in the present study, we found that the expression level of miR-93 was significantly reduced in colon cancer compared with normal colonic mucosa.…”

Section: Discussioncontrasting

confidence: 66%

Clinical significance of microRNA-93 downregulation in human colon cancer

Xiao

Deng

Yang-de

et al. 2013

European Journal of Gastroenterology & Hepatology

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Section: Discussioncontrasting

confidence: 66%

Clinical significance of microRNA-93 downregulation in human colon cancer

Xiao

Deng

Yang-de

et al. 2013

European Journal of Gastroenterology & Hepatology

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“…Our recent results demonstrated miR-93 overexpression involved in cell growth and invasion through downstream regulation of E2F1 transcription factor (11). Other studies recognized miR-34 as a direct target of p53 (12).…”

Section: Introductionsupporting

confidence: 52%

miRNA expression profile in human osteosarcoma: Role of miR-1 and miR-133b in proliferation and cell cycle control

Novello

Pazzaglia

Cingolani

et al. 2012

International Journal of Oncology

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104

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Abstract. miRNA profile deregulation affecting downstream signaling pathways activates endpoints that represent potential biomarkers for prognosis and treatment of tumor patients. In the past 20 years conventional therapy for osteosarcoma (OS) reached a survival plateau, highlighting the need for new therapeutic approaches. In this study, microarray unsupervised and supervised analysis identified, respectively, 100 and 40 differentially expressed miRNAs in OS samples with different grades of malignancy compared to normal bone. When analyzing low-grade and high-grade OS by unsupervised analysis, 12 miRNAs were found to be differentially expressed. Real-time PCR performed on a larger series of OS confirmed a significant lower expression of miR-1, miR-133b and miR-378 * in tumors with respect to control, also showing lower mRNA levels in 31 high-grade OS than in 25 low-grade and in metastatic versus non-metastatic patients. We demonstrated that miR-1 and miR133b were downregulated in OS cell lines compared to normal osteoblasts. Secondly, by transfection with miRNA precursor molecules, we demonstrated that the ectopic expression of miR-1 and miR-133b in U2-OS cell lines significantly reduced cell proliferation and MET protein expression and negatively regulated cell invasiveness and motility in a short-term assay. Cell cycle distribution revealed block in G 1 and delay of cell cycle progression associated with increased apoptosis in miR-1-and miR-133b-transfected cells, respectively. Our data assessed specific miRNA profiling deregulation in OS clinical samples and suggest that the expression of miR-1 and miR-133b may control cell proliferation and cell cycle through MET protein expression modulation. IntroductionOsteosarcoma (OS) is a rare malignant bone neoplasm for which biologic and pathologic information are still largely incomplete. OS has multiple genetic risk factors (1) and is characterized by complex chromosomal abnormalities and genetic cell heterogeneity that in over 70% provide a complex karyotype and drug resistance (2). MicroRNAs (miRNAs) are endogenous non-coding RNAs of 19-24 nucleotides that interacting with the 3' untranslated region (UTR) of mRNA target induce mRNA cleavage when pairing is complete and protein synthesis repression when pairing is incomplete. The relationship between miRNAs and their targets shows combinatorial complication, in terms of both target multiplicity and signal integration (3). MiRNAs are differentially expressed in relation to the developmental state, cell type and tissue (4-6). In literature, there are approximately 1,000 miRNA molecules per cell, with some cells exceeding 50,000 molecules (7). miRNA expression follows a dynamic range and this underscores the regulatory functional importance of miRNAs (3). Recent studies indicate that miRNAs called 'oncomirs' can function either as tumor suppressors or as oncogenes (8).Interconnection between miRNA and cancer is even more evident when analyzing the genomic location of known miRNA genes, more than 50% are in cancer-as...

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“…*P < 0.05 vs. sham group; # P < 0.05 vs. I/R + miR control group Until now, studies of miR-93 have been focused mainly on its involvement in many types of human cancers, such as glioblastoma, gastric cancer, breast carcinoma, and others. miR-93 is overexpressed in a number of types of human cancers and functions as an oncogene by targeting important cancer-related genes [25][26][27][28][29], whereas, in some types of cancers miR-93 was down-regulated and repressed proliferation paradoxically [30,31]. However, the present study is the first to investigate its role in ischemia-induced cerebral injury.…”

Section: Mir-93 Antagomir Induced Ho-1 Expression Through Nrf2mentioning

confidence: 66%

MicroRNA-93 Downregulation Ameliorates Cerebral Ischemic Injury Through the Nrf2/HO-1 Defense Pathway

Wang

Liang

et al. 2016

Neurochem Res

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The present study was designed to evaluate the potential role of miR-93 in cerebral ischemic/reperfusion (I/R) injury in mice. The stroke model was produced in C57BL/6 J mice via middle cerebral artery occlusion (MCAO) for 1 h followed by reperfusion. And miR-93 antagomir was transfected to down-regulate the miR-93 level. Our results showed that miR-93 levels in the cerebral cortex of mice increased at 24 and 48 h after reperfusion. Importantly, in vivo study demonstrated that treatment with miR-93 antagomir reduced cerebral infarction volume, neural apoptosis and restored the neurological scores. In vitro study demonstrated that miR-93 antagomir attenuated hydrogen peroxide (HO)-induced injury. Moreover, miR-93 antagomir suppressed oxidative stress in I/R brain and HO treated cortical neurons. Furthermore, we founded that down-regulation of miR-93 increased the expression of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase-1 (HO-1) and the luciferase reporter assay confirmed that miR-93 directly binds to the predicted 3'-UTR target sites of the nrf2 gene. Finally, we found that knockdown of Nrf2 or HO-1 abolished miR-93 antagomir-induced neuroprotection against oxidative stress in HO treated neuronal cultures. These results suggested that miR-93 antagomir alleviates ischemic injury through the Nrf2/HO-1 antioxidant pathway.

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MicroRNA cloning and sequencing in osteosarcoma cell lines: differential role of miR-93

Abstract: Although further studies are needed to evaluate miRNA involvement in osteosarcoma progression, miR-93 overexpression seems to play an important role in osteosarcoma cell growth and invasion.

Cited by 43 publications

References 47 publications

Clinical significance of microRNA-93 downregulation in human colon cancer

Clinical significance of microRNA-93 downregulation in human colon cancer

miRNA expression profile in human osteosarcoma: Role of miR-1 and miR-133b in proliferation and cell cycle control

MicroRNA-93 Downregulation Ameliorates Cerebral Ischemic Injury Through the Nrf2/HO-1 Defense Pathway

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