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      MiRNA-429 suppresses the growth of gastric cancer cells in vitro

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          Abstract

          Micro-RNAs (miRNAs) have been found to be implicated in a very wide range of physiological processes. This study was aimed to investigate the regulation of miRNA-429 (miR-429) in gastric cancer cells on cell proliferation and apoptosis. Quantitative PCR was employed to detect the expressions of miR-429 after eukaryotic expression plasmid of miR-429 and its inhibitor were transiently transfected into poorly differentiated human gastric cancer cell line BGC823. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction assays were used to examine proliferation ability. Apoptosis was analyzed by flow cytometry after transfection. The results showed that 48 h after transfection, overexpression of miR-429 reached maximum efficiency. Compared with mock transfection, miR-429 inhibited tumor cell proliferation significantly ( P < 0.05) at 48 h and 72 h. of Overexpression of miR-429 promoted tumor cell apoptosis when compared with mock transfected cells ( P < 0.05). On the contrary, miR-429 inhibitor promoted tumor cell proliferation and inhibited apoptosis when compared with controls ( P < 0.05). Our results suggested that miRNA-429 may serve as a tumor suppressor during tumorigenesis of gastric cancer and may be a potential gastric cancer therapeutic target.

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          miR-21-mediated tumor growth.

          MicroRNAs (miRNAs) are approximately 22 nucleotide non-coding RNA molecules that regulate gene expression post-transcriptionally. Although aberrant expression of miRNAs in various human cancers suggests a role for miRNAs in tumorigenesis, it remains largely unclear as to whether knockdown of a specific miRNA affects tumor growth. In this study, we profiled miRNA expression in matched normal breast tissue and breast tumor tissues by TaqMan real-time polymerase chain reaction miRNA array methods. Consistent with previous findings, we found that miR-21 was highly overexpressed in breast tumors compared to the matched normal breast tissues among 157 human miRNAs analysed. To better evaluate the role of miR-21 in tumorigenesis, we transfected breast cancer MCF-7 cells with anti-miR-21 oligonucleotides and found that anti-miR-21 suppressed both cell growth in vitro and tumor growth in the xenograft mouse model. Furthermore, this anti-miR-21-mediated cell growth inhibition was associated with increased apoptosis and decreased cell proliferation, which could be in part owing to downregulation of the antiapoptotic Bcl-2 in anti-miR-21-treated tumor cells. Together, these results suggest that miR-21 functions as an oncogene and modulates tumorigenesis through regulation of genes such as bcl-2 and thus, it may serve as a novel therapeutic target.
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            miR-141 and miR-200a act on ovarian tumorigenesis by controlling oxidative stress response.

            Although there is evidence that redox regulation has an essential role in malignancies, its impact on tumor prognosis remains unclear. Here we show crosstalk between oxidative stress and the miR-200 family of microRNAs that affects tumorigenesis and chemosensitivity. miR-141 and miR-200a target p38α and modulate the oxidative stress response. Enhanced expression of these microRNAs mimics p38α deficiency and increases tumor growth in mouse models, but it also improves the response to chemotherapeutic agents. High-grade human ovarian adenocarcinomas that accumulate miR-200a have low concentrations of p38α and an associated oxidative stress signature. The miR200a-dependent stress signature correlates with improved survival of patients in response to treatment. Therefore, the role of miR-200a in stress could be a predictive marker for clinical outcome in ovarian cancer. In addition, although oxidative stress promotes tumor growth, it also sensitizes tumors to treatment, which could account for the limited success of antioxidants in clinical trials.
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              Functional links between clustered microRNAs: suppression of cell-cycle inhibitors by microRNA clusters in gastric cancer

              microRNAs (miRNAs) play integral roles in diverse processes including tumorigenesis. miRNA gene loci are often found in close conjunction, and such clustered miRNA genes are transcribed from a common promoter to generate polycistronic primary transcript. The primary transcript (pri-miRNA) is then processed by two RNase III proteins to release the mature miRNAs. Although it has been speculated that the miRNAs in the same cluster may play related biological functions, this has not been experimentally addressed. Here we report that the miRNAs in two clusters (miR-106b∼93 ∼ 25 and miR-222 ∼ 221) suppress the Cip/Kip family members of Cdk inhibitors (p57Kip2, p21Cip1 and p27Kip1). We show that miR-25 targets p57 through the 3′-UTR. Furthermore, miR-106b and miR-93 control p21 while miR-222 and miR-221 regulate both p27 and p57. Ectopic expression of these miRNAs results in activation of Cdk2 and facilitation of G1/S phase transition. Consistent with these results, both clusters are abnormally upregulated in gastric cancer tissues compared to the corresponding normal tissues. Ectopic expression of miR-222 cluster enhanced tumor growth in the mouse xenograft model. Our study demonstrates the functional associations between clustered miRNAs and further implicates that effective cancer treatment may require a combinatorial approach to target multiple oncogenic miRNA clusters.
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                Author and article information

                Journal
                J Biomed Res
                J Biomed Res
                JBR
                Journal of Biomedical Research
                Editorial Department of Journal of Biomedical Research
                1674-8301
                September 2012
                20 September 2012
                : 26
                : 5
                : 389-393
                Affiliations
                [a ]Department of Surgical Oncology, the First Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China;
                [b ]Department of Genetics and Molecular Biology, Medical School of Xi'an Jiaotong University/Key Laboratory of Environment and Genes Related Diseases of Ministry of Education, Xi'an, Shaanxi 710061, China.
                Author notes
                *Corresponding author: Chen Huang, Ph.D., Department of Genetics and Molecular Biology, Medical School of Xi'an Jiaotong University/Key Laboratory of Environment and Genes Related Diseases of Ministry of Education, 76 Yanta West Road, Xi'an, Shaanxi 710061, China. Tel:+86-29-82655077, hchen@ 123456mail.xjtu.edu.cn ; Chengxue Dang, M.D., Department of Surgical Oncology, the First Affiliated Hospital, Medical School of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi 710061, China, Tel: +86-29-85324612, dangchengxue@ 123456yahoo.com.cn .
                Article
                jbr-26-05-389
                10.7555/JBR.26.20120029
                3597780
                23554776
                ab0eda18-31d5-4ea1-bc3e-d1cd5ede78aa
                © 2012 by the Journal of Biomedical Research. All rights reserved.

                This work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/

                History
                : 15 May 2012
                : 18 June 2012
                : 29 July 2012
                Categories
                Research Paper

                microrna,gastric cancer,cell cycle,apoptosis
                microrna, gastric cancer, cell cycle, apoptosis

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