Low expression of miR-1469 predicts disease progression and unfavorable post-surgical clinical outcomes in patients with esophageal squamous cell cancer

Liu, Jin; Wang, Chuifang; Liu, Xiangyan; Wang, Yu; Ren, Guohua; Zhu, Luyi; Chen, Zhitao

doi:10.3892/ol.2017.5957

Cited by 10 publications

(7 citation statements)

References 29 publications

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“…MicroRNAs (miRNAs) are defined as a group of short noncoding RNAs that modulate gene expression by controlling either translation restriction or RNA degradation from the posttranscriptional level (Sonkoly, Stahle, & Pivarcsi, ). Some investigations have demonstrated that a multitude of miRNAs have been observed in humans and animals, many of which are suggested to be important in the development of different diseases, including cardiovascular diseases (Liu et al, ; Pirola, Gianotti, Castano, & Sookoian, ; Xie et al, ). Furthermore, some circulating miRNAs are mainly expressed in CAD patients (Labbaf et al, ; Wang et al, ).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of microRNA‐218 reduces cardiac microvascular endothelial cells injury induced by coronary artery disease through the inhibition of HMGB1

Gao¹,

Cui

et al. 2019

Journal Cellular Physiology

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This study is performed to examine the impacts of microRNA-218 (miR-218) on cardiac microvascular endothelial cells (CMECs) injury induced by coronary artery disease (CAD). Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) was applied for detecting miR-218 expression in serum of patients with CAD and healthy controls, and the correlation between miR-218 expression and the clinical indexes such as creatine kinase, creatine kinase-myocardial band, cardiac troponin I, and coronary Gensini score was analyzed. CMECs were coincubated with homocysteine for 24 hr for CMECs injury, and the cells were transfected with miR-218 mimics or miR-218 inhibitors. Besides, we used oxidized low density lipoprotein as an inducer to incubate with CMECs for 24 hr, and the model of CMECs injury was established to be transfected with miR-218 mimics. RT-qPCR and western blot analysis were used to detect miR-218 and HMGB1 expression in CMECs.

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Section: Introductionmentioning

confidence: 99%

Upregulation of microRNA‐218 reduces cardiac microvascular endothelial cells injury induced by coronary artery disease through the inhibition of HMGB1

Gao¹,

Cui

et al. 2019

Journal Cellular Physiology

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“…Through decades of investigations, thousands of miRNAs have been found in humans and animals, among which a notable proportion of miRNAs are found to be critical in the pathogenesis of various diseases, including cardiovascular diseases [9,10,11,12,13,14]. Moreover, some circulating miRNAs predominantly express in CAD patients [15,16].…”

Section: Introductionmentioning

confidence: 99%

miR-126 in Peripheral Blood Mononuclear Cells Negatively Correlates with Risk and Severity and is Associated with Inflammatory Cytokines as well as Intercellular Adhesion Molecule-1 in Patients with Coronary Artery Disease

Zhang²

2018

Cardiology

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Objectives: The aim of this study was to evaluate the association of miR-126 with risk and severity of coronary artery disease (CAD) as well as its correlation with inflammatory cytokines and endothelial related proteins. Methods: In total, 215 patients suspected of CAD who underwent coronary angiography were enrolled in this case control study and were divided into a CAD group (n = 119) and control group (n = 96). miR-126 relative expression was assessed by real-time polymerase chain reaction. Results: The relative expression of miR-126 decreased in CAD patients compared to controls (p < 0.001), and the receiver operating characteristic curve showed a good diagnostic value of miR-126 for CAD risk with an area under the curve of 0.801 (95% CI 0.740-0.861). Additionally, miR-126 was negatively correlated with high-sensitivity C-reactive protein levels (p < 0.001) and reversely associated with TNF-α (p = 0.008) and IL-6 (p < 0.001) levels, while it was positively correlated with the IL-10 level (p < 0.001). In addition, miR-126 was negatively associated with intercellular adhesion molecule-1 (ICAM-1) levels (p = 0.001), and no association of miR-126 with vascular endothelial growth factor was detected (p = 0.142). Meanwhile, the miR-126 relative level was negatively associated with the Gensini score (p < 0.001). Conclusions: Peripheral blood mononuclear cell miR-126 predicts risk and severity and correlates with inflammatory cytokines as well as ICAM-1 in patients with CAD.

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“…Among them, miRNAs play an important role in the occurrence and development of tumors. Different miRNAs, some as proto-oncogenes and some as tumor suppressor genes, can regulate the proliferation, invasion and apoptosis of tumor cells (Liu et al, 2017;.…”

Section: Introductionmentioning

confidence: 99%

Study on Forsythin promoting apoptosis of laryngeal carcinoma cells by regulating miRNA-1469

et al. 2022

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Objective: The paper aimed to explore the mechanism of Forsythin regulating miRNA expression in laryngeal carcinoma cells, and to clarify the molecular biological mechanism of Forsythin regulating miRNA to promote the apoptosis of laryngeal carcinoma cells, providing theoretical and experimental basis for clinical application of Forsythin as an anti-laryngeal cancer treatment drug. Methods: A miR-1469 low-expression laryngeal carcinoma cell line was established. Western blot and flow cytometry were applied to detect the effect of Forsythin on cell apoptosis. Western blot was employed to detect the effects of Forsythin on P53 protein, P53 low expression, and P53 overexpression in laryngeal carcinoma cells, as well as the effects on overexpression of miRNA-1469, and on double low expression of P53 and Mcl1. Real-time PCR method was used to detect the effect of miR-1469 on p53 low expression in laryngeal carcinoma cells. Results: Flow cytometry detection of cell apoptosis showed that, after the cells with low miR-1469 expression were treated with Forsythin, the apoptosis rate was significantly reduced. Western blot detection showed that, compared with the Control group, the expression level of miR-1469 was significantly reduced after Forsythin administration in Hep2 cells with low expression of P53. Compared with the idle Control group, the apoptosis level of laryngeal carcinoma cells in Hep2 cells with low expression of P53 was significantly reduced. In Hep2 cells transfected with P53 overexpression plasmids, apoptosis level of laryngeal carcinoma cells increased. Compared with the idle Control group, the apoptosis level of laryngeal carcinoma cells in the single-transformed P53 shRNA group decreased, while the apoptosis level of the double-transformed miR-1469 mimic+P53 shRNA group increased again. After drug treatment, the apoptosis level of the single-transformed P53 shRNA group decreased, while the apoptosis level of the double-transformed Mcl1 shRNA+P53 shRNA group increased again. Conclusion: Forsythin can promote the apoptosis of laryngeal carcinoma cells by up-regulating the expression of miR-1469 and then down-regulating the expression of Mcl1. The drug can up-regulate the expression of miR-1469 by elevating the expression of P53. miR-1469 can promote the apoptosis of laryngeal carcinoma cells by inhibiting the expression of its downstream target gene Mcl1.

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Low expression of miR-1469 predicts disease progression and unfavorable post-surgical clinical outcomes in patients with esophageal squamous cell cancer

Cited by 10 publications

References 29 publications

Upregulation of microRNA‐218 reduces cardiac microvascular endothelial cells injury induced by coronary artery disease through the inhibition of HMGB1

Upregulation of microRNA‐218 reduces cardiac microvascular endothelial cells injury induced by coronary artery disease through the inhibition of HMGB1

miR-126 in Peripheral Blood Mononuclear Cells Negatively Correlates with Risk and Severity and is Associated with Inflammatory Cytokines as well as Intercellular Adhesion Molecule-1 in Patients with Coronary Artery Disease

Study on Forsythin promoting apoptosis of laryngeal carcinoma cells by regulating miRNA-1469

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