MiR-18b suppresses high-glucose-induced proliferation in HRECs by targeting IGF-1/IGF1R signaling pathways

Wu, Jinhui; Wang, Yi-han; Wang, Wei; Shen, Wei; Sang, Yanzhi; Liu, Lin; Chen, Cuimin

doi:10.1016/j.biocel.2016.02.002

Cited by 35 publications

(28 citation statements)

References 49 publications

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“…This indicates that miR-20b directly targets AKT3 and modulates VEGF-mediated changes in DR [ 76 ]. Wu et al found that the decrease in miR-18b , in HG-induced HRECs, promotes cell proliferation and production of VEGF [ 77 ]. Further, miR-18b performs its function by targetting IGF-1 directly.…”

Section: Roles Of Mirnas In Drmentioning

confidence: 99%

Roles of miRNAs and long noncoding RNAs in the progression of diabetic retinopathy

Gong

2017

Bioscience Reports

101

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Diabetic retinopathy (DR) is the leading cause of blindness in working-age adults across the world. The pathogenesis of DR is multifactorial and the molecular mechanisms are still not fully understood. Accumulating evidence has demonstrated that noncoding RNAs (ncRNAs) may be aberrantly expressed and may play vital roles in the development of DR. Amongst ncRNAs, miRNAs and long ncRNAs (lncRNAs) are known for their regulatory functions. Here, we summarize the functions and mechanisms of known aberrantly expressed miRNAs and lncRNAs in DR. Additionally, a novel lncRNA–mRNA–miRNA network is included in this review. We highlight original studies that provide detailed data about the mechanisms of miRNAs and lncRNAs, their applications as diagnostic or prognostic biomarkers, and their potential therapeutic targets. In conclusion, this review will help us gain a better understanding of the molecular mechanisms by which miRNAs and lncRNAs perform their functions in DR, and provide general strategies and directions for future research.

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Section: Roles Of Mirnas In Drmentioning

confidence: 99%

Roles of miRNAs and long noncoding RNAs in the progression of diabetic retinopathy

Gong

2017

Bioscience Reports

101

View full text Add to dashboard Cite

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“…In addition, IGF-1 could bind with ER (estrogen receptor) or PR (progesterone receptor) to promote tumorigenesis and tumor growth in breast cancer 28 , 29 . Although multiple miRNAs, such as miR-122 30 , miR-18b 31 , miR-515-5p 32 , miR-148a and miR-152 10 , 14 , are involved in IGF-1 regulation pathway by directly targeting IGF-1, IGF-1R, IRS-1 or FOXO3a in breast cancer, the effects of IGF-1 induced signaling cascades on miRNA expression in breast cancer has yet to be evaluated.…”

Section: Introductionmentioning

confidence: 99%

IGF-1-mediated PKM2/β-catenin/miR-152 regulatory circuit in breast cancer

Wen

Liu

Sun

et al. 2017

Sci Rep

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Dysregulation of miRNAs is important in breast cancer initiation and malignant progression. Recently we showed that miR-152 downregulation is associated with breast cancer development, yet the underlying mechanism of miR-152 remains to be well elucidated. In this study, we identified β-catenin as a new direct target of miR-152. MiR-152 inhibited cell proliferation by targeting and inhibiting both β-catenin and PKM2 expression. We found that miR-152 expression sensitized the breast cancer cells to paclitaxel treatment by inhibiting β-catenin and PKM2 expression. Intriguingly, IGF-1 induced β-catenin and PKM2 expression and enhanced β-catenin and PKM2 interaction. Subsequently, IGF-1-induced β-catenin and PKM2 complex translocated into the nucleus, which in turn activated expression of miR-152. These results suggested a regulatory circuit between miR-152, β-catenin and PKM2 in breast cancer. By using human clinical specimens, we also showed that miR-152 expression levels were negatively correlated with β-catenin and PKM2 levels in breast cancer tissues. Our findings provide new insights into a mechanism of miR-152 involved in β-catenin and PKM2 inhibition which would have clinical implication for the cancer development and new treatment option in the future.

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“…Wang et al 18 reported that miRNA-320 was upregulated in the sera and tissues from diabetic rats, as well as in vascular endothelial cells cultured in the presence of HG, and changing miRNA-320 by transfection altered the proliferation and migration of endothelial cells, confirming that miRNA-320 can suppress the proliferation of endothelial cells. 19 All these studies have shown that the role of miRNAs in cardiovascular endothelial dysfunction in diabetes has been acknowledged by many researchers, although cardiovascular diseases due to diabetes remain a major health problem unresolved. HG can reduce miRNA-18b in retinal microvascular endothelial cells, and thus increase the secretion of insulin-like growth factor 2 (IGF-1) and vascular endothelial growth factor (VEGF), so as to regulate the proliferation and apoptosis of endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Hsa‐miRNA‐29a protects against high glucose‐induced damage in human umbilical vein endothelial cells

Huang

et al. 2018

J of Cellular Biochemistry

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Sustained exposure to high glucose (HG) results in dysfunction of vascular endothelial cells. Hence, diabetic patients often suffer from secondary vascular damages, such as vascular sclerosis and thrombogenesis, which may eventually cause cardiovascular problems. Thus, elucidating how HG results in vascular endothelial cell damage and finding an approach for prevention are important to prevent and treat vascular damages in diabetic patients. In the current study, we first showed that 72‐hour exposure to HG‐decreased hsa‐miRNA‐29a and increased the expression of Bcl‐2 associated X protein (Bax), which subsequently inhibited Bcl‐2 and promoted the expression of apoptotic protease activating factor‐1 and activation of caspase‐3, thus directly triggering the mitochondrial apoptotic pathway in human umbilical vein endothelial cells (HUVECs). Study of the underlying mechanism showed that hsa‐miRNA‐29a/Bax plays an essential role in the decreased proliferation and increased apoptosis of HUVECs induced by HG, and overexpression of hsa‐miRNA‐29a effectively inhibits HG‐induced apoptosis and restores the proliferation and tube formation of HUVECs exposed to HG by inhibiting its target gene Bax. In short, our study demonstrates that hsa‐miRNA‐29a is a promising target for the prevention and treatment of vascular injury in diabetic patients.

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MiR-18b suppresses high-glucose-induced proliferation in HRECs by targeting IGF-1/IGF1R signaling pathways

Cited by 35 publications

References 49 publications

Roles of miRNAs and long noncoding RNAs in the progression of diabetic retinopathy

Roles of miRNAs and long noncoding RNAs in the progression of diabetic retinopathy

IGF-1-mediated PKM2/β-catenin/miR-152 regulatory circuit in breast cancer

Hsa‐miRNA‐29a protects against high glucose‐induced damage in human umbilical vein endothelial cells

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