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      miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R

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          Abstract

          Purpose

          Our research aimed to illuminate the role of miR-100-5p in chordoma and potential mechanism.

          Materials and Methods

          We used microRNA array analysis to explore differentially expressed miRNAs in chordoma tissue and then verified by qRT-PCR. Cell proliferation and transwell assay were used to evaluate the function of miR-100-5p. Cell apoptosis was analyzed by flow cytometry, and using biological software, we predicted that the insulin-like growth factor 1 receptor (IGF1R) could be the target gene of miR-100-5p, which was then validated by dual luciferase assays and Western blot.

          Results

          miR-100-5p was downregulated in chordoma tissues. Overexpression of miR-100-5p could suppress the growth of chordoma both in vitro and in vivo, and miR-100-5p could inhibit the migration and invasion of chordoma cells partially by suppressing epithelial–mesenchymal transition (EMT). Furthermore, IGF1R was validated as the target gene of miR-100-5p and expressed in most chordoma tissues.

          Conclusion

          In conclusion, our results showed that miR-100-5p was lowly expressed in chordoma and inhibited tumor malignant progression by targeting IGF1R.

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          Most cited references19

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          MicroRNA signature predicts survival and relapse in lung cancer.

          We investigated whether microRNA expression profiles can predict clinical outcome of NSCLC patients. Using real-time RT-PCR, we obtained microRNA expressions in 112 NSCLC patients, which were divided into the training and testing sets. Using Cox regression and risk-score analysis, we identified a five-microRNA signature for the prediction of treatment outcome of NSCLC in the training set. This microRNA signature was validated by the testing set and an independent cohort. Patients with high-risk scores in their microRNA signatures had poor overall and disease-free survivals compared to the low-risk-score patients. This microRNA signature is an independent predictor of the cancer relapse and survival of NSCLC patients.
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            Estimation of rat mammary tumor volume using caliper and ultrasonography measurements.

            Mammary tumors similar to those observed in women can be induced in rats by intraperitoneal administration of N-methyl-N-nitrosourea. Determining tumor volume is a useful and quantitative way to monitor tumor progression. In this study, the authors measured dimensions of rat mammary tumors using a caliper and using real-time compound B-mode ultrasonography. They then used different formulas to calculate tumor volume from these tumor measurements and compared the calculated tumor volumes with the real tumor volume to identify the formulas that gave the most accurate volume calculations. They found that caliper and ultrasonography measurements were significantly correlated but that tumor volumes calculated using different formulas varied substantially. Mammary tumors seemed to take on an oblate spheroid geometry. The most accurate volume calculations were obtained using the formula V = (W(2) × L)/2 for caliper measurements and the formula V = (4/3) × π × (L/2) × (L/2) × (D/2) for ultrasonography measurements, where V is tumor volume, W is tumor width, L is tumor length and D is tumor depth.
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              Decreased expression of miR-125b and miR-100 in oral cancer cells contributes to malignancy.

              Altered microRNA (miRNA) expression profiles have been observed in numerous malignancies, including oral squamous cell carcinoma (OSCC). However, their role in disease is not entirely clear. Several genetic aberrations are characteristic of OSCC, with amplification of chromosomal band 11q13 and loss of distal 11q being among the most prevalent. It is not known if the expression levels of miRNAs in these regions are altered or whether they play a role in disease. We hypothesize that the expression of miRNAs mapping to 11q are altered in OSCC because of loss or amplification of chromosomal material, and that this contributes to the development and progression of OSCC. We found that miR-125b and miR-100 are down-regulated in OSCC tumor and cell lines, and that transfecting cells with exogenous miR-125b and miR-100 significantly reduced cell proliferation and modified the expression of target and nontarget genes, including some that are overexpressed in radioresistant OSCC cells. In conclusion, the down-regulation of miR-125b and miR-100 in OSCC appears to play an important role in the development and/or progression of disease and may contribute to the loss of sensitivity to ionizing radiation.
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                Author and article information

                Journal
                Cancer Manag Res
                Cancer Manag Res
                CMAR
                cancmanres
                Cancer Management and Research
                Dove
                1179-1322
                02 June 2020
                2020
                : 12
                : 4129-4137
                Affiliations
                [1 ]Musculoskeletal Tumor Center, Peking University People’s Hospital , Beijing, People’s Republic of China
                [2 ]Beijing Key Laboratory of Musculoskeletal Tumor , Beijing, People’s Republic of China
                [3 ]Department of Orthopedics, Yangzhou University Affiliated Hospital , Yangzhou, People’s Republic of China
                Author notes
                Correspondence: Xiaodong Tang; Wei Guo Musculoskeletal Tumor Center, Peking University People’s Hospital , No. 11 Xizhimen South Street, Beijing100044, People’s Republic of ChinaTel +86 10 8832 4471Fax +86.10.8837.8544 Email tang15877@163.com; guobonetumor@163.com
                Article
                252185
                10.2147/CMAR.S252185
                7293400
                32606920
                21ff41be-9bdf-4195-bb15-22fd85970086
                © 2020 Zhang et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 02 March 2020
                : 13 May 2020
                Page count
                Figures: 4, Tables: 2, References: 23, Pages: 9
                Categories
                Original Research

                Oncology & Radiotherapy
                chordoma,mirna,mir-100-5p,igf1r
                Oncology & Radiotherapy
                chordoma, mirna, mir-100-5p, igf1r

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