Dysregulation of microRNA‑23b‑3p contributes to the development of intracranial aneurysms by targeting phosphatase and tensin homolog

Guo, Dong; Wang, Ye-Wei; Yan, Lei; Ma, Ji; Han, Xinwei; Shui, Shaofeng

doi:10.3892/ijmm.2018.3706

Cited by 5 publications

(3 citation statements)

References 35 publications

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“…Multiple studies have demonstrated the dysregulation of miRNAs in patients with both IA and aSAH [ 23 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 ] ( Table 1 ). However, it is essential to note that the quality of evidence in most of these studies is generally low.…”

Section: Resultsmentioning

confidence: 99%

The Role of Epigenetics in Brain Aneurysm and Subarachnoid Hemorrhage: A Comprehensive Review

Fernández-Pérez,

Macias-Gómez,

Suárez-Pérez

et al. 2024

IJMS

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This comprehensive review explores the emerging field of epigenetics in intracranial aneurysm (IA) and aneurysmal subarachnoid hemorrhage (aSAH). Despite recent advancements, the high mortality of aSAH needs an understanding of its underlying pathophysiology, where epigenetics plays a crucial role. This review synthesizes the current knowledge, focusing on three primary epigenetic mechanisms: DNA methylation, non-coding RNA (ncRNA), and histone modification in IA and aSAH. While DNA methylation studies are relatively limited, they suggest a significant role in the pathogenesis and prognosis of IA and aSAH, highlighting differentially methylated positions in genes presumably involved in these pathologies. However, methodological limitations, including small sample sizes and a lack of diverse population studies, temper these results. The role of ncRNAs, particularly miRNAs, has been more extensively studied, but there are still few studies focused on histone modifications. Despite methodological challenges and inconsistent findings, these studies underscore the involvement of miRNAs in key pathophysiological processes, including vascular smooth muscle regulation and the inflammatory response. This review emphasizes methodological challenges in epigenetic research, advocating for large-scale epigenome-wide association studies integrating genetic and environmental factors, along with longitudinal studies. Such research could unravel the complex mechanisms behind IA and aSAH, guiding the development of targeted therapeutic approaches.

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Section: Resultsmentioning

confidence: 99%

The Role of Epigenetics in Brain Aneurysm and Subarachnoid Hemorrhage: A Comprehensive Review

Fernández-Pérez,

Macias-Gómez,

Suárez-Pérez

et al. 2024

IJMS

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“…Recently, miR-23b-3p has been specifically linked to various functions in various cancers through a cell-type-specific manner. In various kinds of tumors, miR-23b-3p was reported to act as a tumor suppressor [ 34 , 35 ]. In this study, miR-23b-3p expression level was markedly reduced in COAD tissues compared with adjacent normal colonic tissues and significantly downregulated in all four COAD cell lines (SW620, SW1116, CW-2, and LoVo) analyzed relative to its expression in a normal colonic epithelial cell NCM460.…”

Section: Discussionmentioning

confidence: 99%

miR-23b-3p Inhibits the Oncogenicity of Colon Adenocarcinoma by Directly Targeting NFE2L3

Huang

Yang

et al. 2021

Journal of Oncology

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Background and Aims. MicroR-23b-3p (miR-23b-3p) has been found to be abnormally expressed in a variety of malignant tumors and to play a role in tumor inhibition or promotion. However, the regulatory mechanism of miR-23b-3p in COAD remains unclear. The purpose of this study was to investigate the clinical significance of miR-23b-3p expression in COAD cells and to explore its role and regulatory mechanism in the growth of COAD. Materials and Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure miR-23b-3p expression in COAD tissues and cell lines. After transfecting miR-23b-3p mimics into two human COAD cell lines (SW620 and LoVo), the cell counting kit-8 (CCK-8), colony formation, and 5-ethynyl-2′-deoxyuridine (EdU) assays were used to detect cell proliferation, the Transwell assay was used to measure cell migration and invasion capacity, and flow cytometry was used to evaluate cell apoptosis in vitro. In addition, a luciferase reporter assay was used to determine whether miR-23b-3p targets NFE2L3. The downstream regulatory mechanisms of miR-23b-3p action in COAD cells were also investigated. For in vivo tumorigenesis assay, COAD cells stably overexpressing miR-23b-3p were injected subcutaneously into the flank of nude mice to obtain tumors. Results. Significantly decreased expression of miR-23b-3p was detected in COAD tissues and cell lines. Exogenous miR-23b-3p expression inhibited cell proliferation, migration, and invasion and promoted cell apoptosis of COAD cells in vitro. Nuclear factor erythroid 2 like 3 (NFE2L3) was identified as a direct target gene of miR-23b-3p. In addition, reintroduction of NFE2L3 partially abolished the anticancer effects of miR-23b-3p on COAD cells. Furthermore, miR-23b-3p overexpression hindered the growth of COAD cells in vivo. Conclusion. miR-23b-3p inhibited the oncogenicity of COAD cells in vitro and in vivo by directly targeting NFE2L3, suggesting the importance of the miR-23b-3p/NFE2L3 pathway in the development of COAD.

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“…Interestingly, the levels of several miRNAs (e.g., miR-143, miR-145, and miR-23b) were found to be consistently down-regulated among the studies described above [30,45,47,54]. For example, miR-23b was reduced in IA tissues and was reported to target phosphatase and tensin homolog (PTEN) [55], a key regulator of proliferation, differentiation, and cytokine production during pathological vascular remodeling in smooth muscle cells [56]. MiR-143 and miR-145 play an important role in controlling vascular smooth muscle phenotype by maintaining or inhibiting differentiation [28,57] and were found to be significantly down-regulated in IA tissues and plasma [30,44,45,47,54,57].…”

Section: Mirna In Intracranial Aneurysmal (Ia) Tissue and Subarachnoid Hemorrhagementioning

confidence: 95%

MicroRNAs as Biomarkers for Predicting Complications following Aneurysmal Subarachnoid Hemorrhage

Wang

Springer

Hatton

2021

IJMS

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Aneurysmal subarachnoid hemorrhage (aSAH) is a high mortality hemorrhagic stroke that affects nearly 30,000 patients annually in the United States. Approximately 30% of aSAH patients die during initial hospitalization and those who survive often carry poor prognosis with one in five having permanent physical and/or cognitive disabilities. The poor outcome of aSAH can be the result of the initial catastrophic event or due to the many acute or delayed neurological complications, such as cerebral ischemia, hydrocephalus, and re-bleeding. Unfortunately, no effective biomarker exists to predict or diagnose these complications at a clinically relevant time point when neurologic injury can be effectively treated and managed. Recently, a number of studies have demonstrated that microRNAs (miRNAs) in extracellular biofluids are highly associated with aSAH and complications. Here we provide an overview of the current research on relevant human studies examining the correlation between miRNAs and aSAH complications and discuss the potential application of using miRNAs as biomarkers in aSAH management.

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Dysregulation of microRNA‑23b‑3p contributes to the development of intracranial aneurysms by targeting phosphatase and tensin homolog

Cited by 5 publications

References 35 publications

The Role of Epigenetics in Brain Aneurysm and Subarachnoid Hemorrhage: A Comprehensive Review

The Role of Epigenetics in Brain Aneurysm and Subarachnoid Hemorrhage: A Comprehensive Review

miR-23b-3p Inhibits the Oncogenicity of Colon Adenocarcinoma by Directly Targeting NFE2L3

MicroRNAs as Biomarkers for Predicting Complications following Aneurysmal Subarachnoid Hemorrhage

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