microRNA-181 serves as a dual-role regulator in the development of human cancers

Rezaei, Tayebeh; Amini, Mohammad; Hashemi, Zahra Sadat; Mansoori, Behzad; Rezaei, Sarah; Karami, Hadi; Mosafer, Jafar; Mokhtarzadeh, Ahad; Baradaran, Behzad

doi:10.1016/j.freeradbiomed.2019.12.043

Cited by 62 publications

(43 citation statements)

References 143 publications

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“…Several studies have demonstrated the effects of miR-181b on the regulation of cell proliferation, invasion and apoptosis in different types of cancer, such as colorectal ( 7 ), ovarian ( 8 ) and cervical cancer ( 9 ). Furthermore, miR-181 has been shown to be involved in the regulation of tumor growth and the immune system by engaging factors involved in signaling pathways, such as mitogen-activated protein kinase 1 (MAPK1) ( 10 ) and nuclear factor-κB (NF-κB) ( 11 ). However, the biological functions of miR-181b in regulating the NF-κB signaling pathway in colon cancer remain largely unclear.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of miR‑181b inhibits human colon�cancer cell proliferation by targeting CYLD and inhibiting the NF‑κB signaling pathway

et al. 2020

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It has been repor ted that m icroR NA (miRNA/miR)-181b plays an important role in regulating cellular proliferation, invasion and apoptosis in various tumors. However, the role of miR-181b and its molecular mechanisms in colon cancer cells have not yet been elucidated. The present study thus aimed to investigate the mechanisms of miR-181b targeting cylindromatosis (cYLd) to regulate the nuclear factor-κB (NF-κB) signaling pathway, and to determine its role in colon cancer cell proliferation and apoptosis. For this purpose, miR-181b was overexpressed and silenced in the SW480 cell line. The cell proliferation and apoptotic rates were determined using a cell counting kit and colony formation assays, and Annexin V-FITc staining, respectively. The expression levels of proteins associated with the NF-κB signaling pathway and apoptosis were detected by western blot analysis. Furthermore, a dual luciferase assay was applied to confirm the interaction between miR-181b and CYLD. CYLD was also overexpressed and silenced in the SW480 cell line using a cYLd overexpression plasmid and siRNA technology, respectively. Transfected cells were used for subsequent experiments. In addition, a nude mouse model was established to measure tumor volume and weight. Immunohistochemistry and a TUNEL assay were performed to detect the Ki67 levels and the cell apoptotic rate, respectively. compared with the control group, miR-181 silencing or cYLd overexpression significantly attenuated cell proliferation, invasion and migration, and notably increased the proportion of apoptotic cells. Furthermore, the expression levels of Bax and cleaved caspase-3 were markedly increased, whereas those of Bcl-2 were significantly decresaed (P<0.05). In addition, the protein expression levels of p-p65/p65 and p-IκBα/IκBα were significantly downregulated and upregulated, respectively (P<0.05). consistent with the results obtained in vitro, in vivo experiments using a nude mouse model yielded similar findings. The aforementioned results indicated that miR-181b downregulation inhibited human colon cancer cell proliferation by targeting cYLd to attenuate the activity of the NF-κB signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Downregulation of miR‑181b inhibits human colon�cancer cell proliferation by targeting CYLD and inhibiting the NF‑κB signaling pathway

et al. 2020

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“…Of note, some miRNAs serve dual roles, even in a type of cancer. For example, miR-181 family consists of four members miR-181a to miR-181d that exhibit inconsistent expression in many solid cancers, indicating they might be onco-miRNAs as well as tumour suppressor miRNAs [60]. It is intriguing that those members of miR-181 family are located at different clusters of chromosomes and subject to different epigenetic modifications, suggesting that miRNA biogenesis can be modified by other epigenetic modifications.…”

Section: Intratumor Epigenetic Alterationsmentioning

confidence: 99%

Epigenetic regulation in human cancer: the potential role of epi-drug in cancer therapy

et al. 2020

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Epigenetics is dynamic and heritable modifications to the genome that occur independently of DNA sequence. It requires interactions cohesively with various enzymes and other molecular components. Aberrant epigenetic alterations can lead to inappropriate onset of genetic expressions and promote tumorigenesis. As the epigenetic modifiers are susceptible to extrinsic factors and reversible, they are becoming promising targets in multiple cancer therapies. Recently, various epi-drugs have been developed and implicated in clinical use. The use of epi-drugs alone, or in combination with chemotherapy or immunotherapy, has shown compelling outcomes, including augmentation of anti-tumoral effects, overcoming drug resistance, and activation of host immune response.

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“…We focused on the miR-181 family and miR-484 because these miRs are known to be associated with the mitochondrial function of cardiomyocytes. Members of the miR-181 family are multifunctional miRs 7) that were originally identified as specifically expressed in haematopoietic cells and modulate haematopoietic lineage differentiation. 8) A series of experimental studies by Das et al [9][10][11] showed that members of the miR-181 family (miR-181a, b, and c) modulate the myocardial response to oxidative stress in cardiomyocytes.…”

Section: Introductionmentioning

confidence: 99%

Potential Association of Circulating MicroRNA-181c and MicroRNA-484 Levels with Cardiorespiratory Fitness after Myocardial Infarction: A Pilot Study

Miyazawa

Iso

Tsujiuchi

et al. 2021

PRM

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In the field of exercise physiology, there has been great interest in exploring circulating microRNAs (miRs) as potential biomarkers. However, it remains to be determined whether circulating miRs reflect cardiorespiratory fitness. The aim of this study was to investigate the association between circulating levels of specific miRs and cardiorespiratory fitness evaluated by cardiopulmonary exercise testing (CPET) after acute myocardial infarction (MI). Methods: Twenty patients who had had an acute MI were included. All patients underwent CPET in the convalescent phase. Quantitative real-time polymerase chain reaction analyses for miR-181 members (a/b/c) and miR-484 were performed to determine the expression levels in the peripheral blood of the included patients and healthy control subjects (n=5). Results: Post-MI patients showed impaired exercise tolerance and ventilatory efficiency in CPET analysis. Compared with controls, circulating levels of miR-181a and 181c were gradually and significantly elevated through the 1st to 7th days after acute MI, whereas miR-181b and miR-484 were not. Circulating miR levels did not correlate with clinical or echocardiographic parameters. However, circulating levels of miR-181c and miR-484 on the 7th day showed significant positive correlations with the anaerobic threshold and peak oxygen consumption from CPET analysis. Moreover, miR-181c levels were inversely associated with the ventilatory inefficiency index. Patients with high exercise capacity after MI showed significantly higher expressions of circulating miR-181c and miR-484 than those with low exercise capacity. Conclusions: The results of this pilot study suggest that circulating levels of miR-181c and miR-484 after acute MI may be predictive biomarkers of post-MI cardiorespiratory fitness.

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microRNA-181 serves as a dual-role regulator in the development of human cancers

Cited by 62 publications

References 143 publications

Downregulation of miR‑181b inhibits human colon�cancer cell proliferation by targeting CYLD and inhibiting the NF‑κB signaling pathway

Downregulation of miR‑181b inhibits human colon�cancer cell proliferation by targeting CYLD and inhibiting the NF‑κB signaling pathway

Epigenetic regulation in human cancer: the potential role of epi-drug in cancer therapy

Potential Association of Circulating MicroRNA-181c and MicroRNA-484 Levels with Cardiorespiratory Fitness after Myocardial Infarction: A Pilot Study

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