MicroRNA-26b inhibits metastasis of osteosarcoma via targeting CTGF and Smad1

Duan, Guoqing; Ren, Chunfeng; Zhang, Yuanmin; Feng, Shiqing

doi:10.1007/s13277-015-3305-6

Cited by 25 publications

(17 citation statements)

References 37 publications

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“…Additionally, miR-26b-5p mimic inhibited Col1a2 and CTGF expression at the post-transcriptional level in cardiac fibroblasts. The present conclusion has been partially supported by previous studies showing that CTGF is a target of miR-26b in osteosarcoma cells35 and in pulmonary artery smooth muscle cells36, respectively. Importantly, our present data validated that circRNA_000203 specifically eliminates the interactions of miR-26b-5p with the 3′-UTRs of Col1a2 and CTGF, and impairs the inhibitory effect of miR-26b-5p on the fibrosis-associated genes, including Col1a2, Col3a1, α-SMA and CTGF, in cardiac fibroblasts.…”

Section: Disccusionsupporting

confidence: 87%

CircRNA_000203 enhances the expression of fibrosis-associated genes by derepressing targets of miR-26b-5p, Col1a2 and CTGF, in cardiac fibroblasts

Tang

Zhang

Huang

et al. 2017

Sci Rep

233

168

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Circular RNAs (circRNAs) participate in regulating gene expression in diverse biological and pathological processes. The present study aimed to investigate the mechanism underlying the modulation of circRNA_000203 on expressions of fibrosis-associated genes in cardiac fibroblasts. CircRNA_000203 was shown upregulated in the diabetic mouse myocardium and in Ang-II-induced mouse cardiac fibroblasts. Enforced-expression of circRNA_000203 could increase expressions of Col1a2, Col3a1 and α-SMA in mouse cardiac fibroblasts. RNA pull-down and RT-qPCR assay indicated that circRNA_000203 could specifically sponge miR-26b-5p. Dual luciferase reporter assay revealed that miR-26b-5p interacted with 3′UTRs of Col1a2 and CTGF, and circ_000203 could block the interactions of miR-26b-5p and 3′UTRs of Col1a2 and CTGF. Transfection of miR-26b-5p could post-transcriptionaly inhibit expressions of Col1a2 and CTGF, accompanied with the suppressions of Col3a1 and α-SMA in cardiac fibroblasts. Additionally, over-expression of circRNA_000203 could eliminate the anti-fibrosis effect of miR-26b-5p in cardiac fibroblasts. Together, our results reveal that suppressing the function of miR-26b-5p contributes to the pro-fibrosis effect of circRNA_000203 in cardiac fibroblasts.

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Section: Disccusionsupporting

confidence: 87%

CircRNA_000203 enhances the expression of fibrosis-associated genes by derepressing targets of miR-26b-5p, Col1a2 and CTGF, in cardiac fibroblasts

Tang

Zhang

Huang

et al. 2017

Sci Rep

233

168

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“…One study reported inclusion and exclusion criteria [39]. Six studies reported randomization [39, 46, 47, 55, 58, 65], whereas 23 studies reported potential conflicts of interest and study funding [25, 33, 36, 37, 39, 40, 43, 44, 46-48, 50, 52-58, 60-62, 64]. Only one study reported blinded assessment of outcome [53].…”

Section: Resultsmentioning

confidence: 99%

“…There were 40 mice in the intervention arm and 57 in the control arm. The tumor volume significantly reduced when the decreased tumor suppressor miRNAs were corrected (pooled MD = [ -4.01]; 95% confidence interval [CI]: [-5.89]- [-2.13]; p < 0.00001; Figure 8A, part 2)in a random-effects model [33, 35, 36, 60, 63, 64]. MiRNAs were infected into the OS cells by lentivirus vectors in 8 studies, and were combined for a meta-analysis.…”

Section: Resultsmentioning

confidence: 99%

MicroRNAs for osteosarcoma in the mouse: a meta-analysis

Chang

Yao

et al. 2016

Oncotarget

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Osteosarcoma (OS) is the most common primary malignant bone carcinoma with high morbidity that happens mainly in children and young adults. As the key components of gene-regulatory networks, microRNAs (miRNAs) control many critical pathophysiological processes, including initiation and progression of cancers. The objective of this study is to summarize and evaluate the potential of miRNAs as targets for prevention and treatment of OS in mouse models, and to explore the methodological quality of current studies. We searched PubMed, Web of Science, Embase, Wan Fang Database, VIP Database, China Knowledge Resource Integrated Database, and Chinese BioMedical since their beginning date to 10 May 2016. Two reviewers separately screened the controlled studies, which estimate the effects of miRNAs on osteosarcoma in mice. A pair-wise analysis was performed. Thirty six studies with enough randomization were selected and included in the meta-analysis. We found that blocking oncogenic or restoring decreased miRNAs in cancer cells could significantly suppress the progression of OS in vivo, as assessed by tumor volume and tumor weight. This meta-analysis suggests that miRNAs are potential therapeutic targets for OS and correction of the altered expression of miRNAs significantly suppresses the progression of OS in mouse models, however, the overall methodological quality of studies included here was low, and more animal studies with the rigourous design must be carried out before a miRNA-based treatment could be translated from animal studies to clinical trials.

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“…La-related protein 1 (LARP1) was identified as a regulatory target of miR-26a/b inhibiting prostate cancer (PCa) cell invasion by Kato et al [37]. Duan and co-workers found that downregulation of miR-26b in osteosarcoma elevates the levels of CTGF and Smad1, facilitating metastasis in osteosarcoma (os) [27]. Reduced miR-26b expression promoted breast fibroblast migration and invasion.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-26b inhibits tumor metastasis by targeting the KPNA2/c-jun pathway in human gastric cancer

et al. 2016

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MicroRNAs (miRNA) play an important role in carcinogenesis. Previously, we identified miR-26b as a significantly downregulated miRNA in gastric cancer (GC) tissues (n = 106) based on differential quantitative RT-PCR (RT-qPCR) miRNA expression profiles. In the current study, we aimed to clarify the potential role of miR-26b and related target genes in GC progression. Downregulation of miR-26b was associated with advanced tumor-node-metastasis stage (TNM stage) and poor 5-year survival rate. Forced expression of miR-26b led to inhibition of GC cell migration and invasion in vitro and lung metastasis formation in vivo. Conversely, depletion of miR-26b had stimulatory effects. Additionally, miR-26b affected GC cell behavior through negative regulation of the metastasis promoter, karyopherin alpha 2 (KPNA2). Ectopic expression of miR-26b induced a reduction in KPNA2 protein levels, confirmed by luciferase assay data showing that miR-26b directly binds to the 3′ untranslated regions (UTR) of KPNA2 mRNA. Furthermore, miR-26b and KPNA2 mRNA/protein expression patterns were inversely correlated in GC tissues. Cag A of Helicobacter pylori (Hp) enhanced miR-26b levels through regulation of the KPNA2/c-jun pathway. Taken together, our data indicate that miR-26b plays an anti-metastatic role and is downregulated in GC tissues via the KPNA2/c-jun pathway. Based on the study findings, we propose that miR-26b overexpression or KPNA2/c-jun suppression may have therapeutic potential in inhibiting GC metastasis.

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MicroRNA-26b inhibits metastasis of osteosarcoma via targeting CTGF and Smad1

Cited by 25 publications

References 37 publications

CircRNA_000203 enhances the expression of fibrosis-associated genes by derepressing targets of miR-26b-5p, Col1a2 and CTGF, in cardiac fibroblasts

CircRNA_000203 enhances the expression of fibrosis-associated genes by derepressing targets of miR-26b-5p, Col1a2 and CTGF, in cardiac fibroblasts

MicroRNAs for osteosarcoma in the mouse: a meta-analysis

MicroRNA-26b inhibits tumor metastasis by targeting the KPNA2/c-jun pathway in human gastric cancer

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