ROCK1-PredictedmicroRNAs Dysregulation Contributes to Tumor Progression in Ewing Sarcoma

Roberto, Gabriela Molinari; Delsin, Lara Elis Alberici; Vieira, Gabriela Maciel; Silva, M O; Hakime, Rodrigo Guedes; Gava, Nelson Fabrício; Engel, Edgard Eduard; Scrideli, Carlos Alberto; Tone, Luíz Gonzaga; Brassesco, María Sol

doi:10.1007/s12253-017-0374-4

Cited by 15 publications

(9 citation statements)

References 31 publications

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“…Therefore, we inferred that miR-124-3p may be an exception in the miR-124 family, and then we collected articles on miR-124 to explore the detailed results. As we found, miR-124-3p directly targeted PDCD6 to inhibit metastasis in breast cancer [15] and cooperated with ROCK1 to reduced procession in Ewing Sarcoma [16]. Luo et al reported that miR-124-3p suppresses glioma aggressiveness by targeting Fra-2 [17].…”

Section: Discussionmentioning

confidence: 78%

Role of MicroRNA-124 as a Prognostic Factor in Multiple Neoplasms: A Meta-Analysis

Zhou

Wang

et al. 2019

Disease Markers

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Objective MicroRNA-124 (miR-124) was revealed to be an attractive prognostic tumour biomarker in recent studies. However, the results remain inconclusive. Hence, this meta-analysis was carried out to clarify the precise predictive value of miR-124. Materials and Methods Relevant studies were searched in PubMed, EMBASE, Web of Science, and the Cochrane Library up to October 2018. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) were extracted from the selected studies. Results A total of 29 articles investigating the correlation between miR-124 expression and prognosis were initially identified. The pooled HR for overall survival (OS) of high miR-124 expression in multiple cancers was 0.55 (95%CI = 0.50–0.61). Disease-free survival (DFS)/progression-free survival (HR = 0.48, 95%CI = 0.38–0.61) revealed a protective role of increased miR-124 expression. Epigenetic hypermethylation of miR-124 mediated the silencing of its expression, which is correlated significantly with unfavourable survival (OS: HR = 2.06, 95%CI = 1.68–2.53; DFS/recurrence-free survival: HR = 2.77, 95%CI = 1.85–4.16). Conclusions Taken together, our results suggest that miR-124 plays an antioncogenic role in various tumors, such as lung cancer and colorectal cancer. If methylation of miR-124 could be prevented, progression and metastasis would be improved; thus, miR-124 may be a promising biomarker and novel therapeutic target. Further large-scale studies are needed to confirm this possible effect.

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Section: Discussionmentioning

confidence: 78%

Role of MicroRNA-124 as a Prognostic Factor in Multiple Neoplasms: A Meta-Analysis

Zhou

Wang

et al. 2019

Disease Markers

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“…In several human cancers, hsa-miR-335 has multiple roles in carcinogenesis [21][22][23][24]. Although little is known of the role of miR-335-3p in lung cancer, in several other cancers, miR-335-3p is down-regulated [25][26][27][28]. The expression of miR-335-3p in adenocarcinoma of the lung and the mechanism remain unknown, and there have been no previous studies on the miR-335-3p/COPB2 axis in adenocarcinoma of the lung or other cancers.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of the Coatomer Protein Complex Subunit beta 2 (COPB2) Gene Targets microRNA-335-3p in NCI-H1975 Lung Adenocarcinoma Cells to Promote Cell Proliferation and Migration

Jiang

et al. 2020

Med Sci Monit

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Departmental sources Background: The coatomer protein complex subunit beta 2 (COPB2) gene is upregulated and promotes cell proliferation in some cancer cells. This study aimed to investigate the role of microRNA (miRNA) targeting by COPB2 gene expression in human lung adenocarcinoma cell lines, including NCI-H1975 cells. Material/Methods: COPB2 expression in normal human bronchial epithelial cells and lung adenocarcinoma cells was measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot. NCI-H1975 human lung adenocarcinoma cells were transfected with short-interfering COPB2 (siCOPB2). Cell apoptosis and cell proliferation were evaluated by flow cytometry and Cell Counting Kit-8 (CCK-8) assays, respectively. The transwell assay evaluated cell migration. Targeting of miR-335-3p by COPB2 was predicted using TargetScan 7.2 and verified using a dual-luciferase reporter assay in NCI-H1975 cells. MiR-335-3p mimics were transfected into NCI-H1975 cells. The further functional analysis included detection of protein expression for cyclin D1, tissue inhibitor matrix metalloproteinase-1 (TIMP-1), matrix metallopeptidase 9 (MMP9), Bcl-2, and Bax, to verify the role of miR-335-3p targeting by COPB2 in lung adenocarcinoma cells. Results: COPB2 was upregulated in lung adenocarcinoma cells and was a direct target of miR-335-3p mimics. COPB2 knockdown promoted cell apoptosis, inhibited cell migration and proliferation in NCI-H1975 cells. The effects of COPB2 knockdown on NCI-H1975 cells were increased by miR-335-3p mimics, which also further reduced the expression levels of cyclin D1, MMP9, and Bcl-2 and further increased TIMP-1 and Bax by siCOPB2. Conclusions: This study showed that COPB2 was the functional target of miR-335-3p in NCI-H1975 human adenocarcinoma cells.

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“…Therefore, miR-335 disturbed proliferation and migration, while promoting radiosensitivity of melanoma by inhibiting ROCK1. The miR-335/ROCK1 axis regulated multiple functions, including tumor progression (19)(20)(21), myocardial ischemia/reperfusion (22), and chondrogenesis (23). Lynch and colleagues firstly illustrated the negative feedback loop among miR-335/ROCK1-noncanonical TGF-β signaling and MYCN (24).…”

Section: Discussionmentioning

confidence: 99%

miR-335 Acts as a Tumor Suppressor and Enhances Ionizing Radiation-Induced Tumor Regression by Targeting ROCK1

Cheng

Shen

2020

Front. Oncol.

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Recent development of integrative therapy against melanoma combines surgery, radiotherapy, targeted therapy, and immunotherapy; however, the clinical outcomes of advanced stage and recurrent melanoma are poor. As a skin cancer, melanoma is generally resistant to radiotherapy. Hence, there is an urgent need for evaluation of the mechanisms of radioresistance. The present study identified miR-335 as one of the differential expression of miRNAs in recurrent melanoma biopsies post-radiotherapy. The expression of miR-335 declined in melanoma tissues compared to the adjacent tissues. Moreover, miR-335 expression correlated with advanced stages of melanoma negatively. Consistent with the prediction of STARBASE and miRDB database, miR-335 targeted ROCK1 via binding with 3 ′ -UTR of ROCK1 directly, resulting in attenuation of proliferation, migration, and radioresistance of melanoma cells. The authors validated that overexpression of miR-335 enhanced X-ray-induced tumor regression by B16 mouse models. Briefly, the present findings gained insights into miR-335/ROCK1-mediated radiosensitivity and provided a promising therapeutic strategy for improving radiotherapy against melanoma.

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ROCK1-PredictedmicroRNAs Dysregulation Contributes to Tumor Progression in Ewing Sarcoma

Cited by 15 publications

References 31 publications

Role of MicroRNA-124 as a Prognostic Factor in Multiple Neoplasms: A Meta-Analysis

Role of MicroRNA-124 as a Prognostic Factor in Multiple Neoplasms: A Meta-Analysis

Upregulation of the Coatomer Protein Complex Subunit beta 2 (COPB2) Gene Targets microRNA-335-3p in NCI-H1975 Lung Adenocarcinoma Cells to Promote Cell Proliferation and Migration

miR-335 Acts as a Tumor Suppressor and Enhances Ionizing Radiation-Induced Tumor Regression by Targeting ROCK1

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