The Regulatory Roles of Non-coding RNAs in Angiogenesis and Neovascularization From an Epigenetic Perspective

Hernández-Romero, Itzel Alejandra; Guerra-Calderas, Lissania; Salgado-Albarrán, Marisol; Maldonado-Huerta, Tatiana; Soto-Reyes, Ernesto

doi:10.3389/fonc.2019.01091

Cited by 35 publications

(21 citation statements)

References 169 publications

(132 reference statements)

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“…They can regulate cancer cell proliferation, migration, and invasion [6]. Also circRNAs can contribute to cancer development through the regulation of angiogenesis and neovascularization [34]. For instance, circRNA MYLK promotes bladder cancer progression and metastasis via enhancing cancer cell growth and angiogenesis [35].…”

Section: Discussionmentioning

confidence: 99%

CircATRNL1 activates Smad4 signaling to inhibit angiogenesis and ovarian cancer metastasis via miR‐378

Wang

Zhou

et al. 2021

Molecular Oncology

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Ovarian cancer is one of the most frequent carcinomas in females, and the occurrence rate is still rising despite many advances made. The pathogenesis of ovarian cancer remains greatly unclear. Here, we investigated the mechanisms of ovarian cancer, with the focus on circATRNL1. Human ovarian cancer tissues and cell lines were used to examine levels of circATRNL1, miR‐378, Smad4, AKT, and other proliferation‐related and migration‐related proteins. Cellular assays were used to determine cancer cell proliferation, invasion, migration, apoptosis, and angiogenesis. We validated the interactions of circATRNL1/miR‐378 and miR‐378/Smad4, and a mouse tumor xenograft model was employed to assess the effect of circATRNL1 on tumor growth and metastasis in vivo. We found that circATRNL1 was decreased while miR‐378 was increased in human ovarian cancer tissues and cells. circATRNL1 bound to miR‐378 while miR‐378 directly targeted Smad4. Overexpression of circATRNL1 or knockdown of miR‐378 suppressed angiogenesis and ovarian cancer cell proliferation, invasion, and migration via decreasing proliferation‐ and migration‐related proteins via miR‐378 or Smad4, respectively. Overexpression of circATRNL1 restrained ovarian cancer growth and abdominal metastasis in vivo. Our findings indicate that circATRNL1 acts as a miR‐378 sponge to active Smad4 signaling and suppresses angiogenesis and ovarian cancer metastasis.

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Section: Discussionmentioning

confidence: 99%

CircATRNL1 activates Smad4 signaling to inhibit angiogenesis and ovarian cancer metastasis via miR‐378

Wang

Zhou

et al. 2021

Molecular Oncology

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“…Growing evidence indicates that miRNAs play a critical role in angiogenic processes [ 160 ]. In particular, miR-424 is expressed in a sequential manner during the endothelial differentiation of DPSCs.…”

Section: Epigenetic Mechanisms In Dpscsmentioning

confidence: 99%

Epigenetic Regulation of Dental Pulp Stem Cell Fate

Zhou

Gan

Yan

et al. 2020

Stem Cells International

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Epigenetic regulation, mainly involving DNA methylation, histone modification, and noncoding RNAs, affects gene expression without modifying the primary DNA sequence and modulates cell fate. Mesenchymal stem cells derived from dental pulp, also called dental pulp stem cells (DPSCs), exhibit multipotent differentiation capacity and can promote various biological processes, including odontogenesis, osteogenesis, angiogenesis, myogenesis, and chondrogenesis. Over the past decades, increased attention has been attracted by the use of DPSCs in the field of regenerative medicine. According to a series of studies, epigenetic regulation is essential for DPSCs to differentiate into specialized cells. In this review, we summarize the mechanisms involved in the epigenetic regulation of the fate of DPSCs.

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“… 161 , 162 Furthermore, various miRNAs mediate the expression of epigenetic elements, such as DNMTs (regulated by miR-152, miR-30, and miR-148a/b), HDACs (regulated by miR-140, miR-1, and miR-449a), and a polycomb group of genes (regulated by miR-101 and miR-26a). 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 Previous studies have indicated that miRNAs are expressed in the vascular system. As shown in Table 1 , numerous studies have indicated that miRNAs impinge on a wide variety of cellular activity networks, related to the ISR biological pathway, including VSMC and EC function.…”

Section: Main Textmentioning

confidence: 99%

Targeting the epigenome in in-stent restenosis: from mechanisms to therapy

Yang

Guo

et al. 2021

Molecular Therapy - Nucleic Acids

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Coronary artery disease (CAD) is one of the most common causes of death worldwide. The introduction of percutaneous revascularization has revolutionized the therapy of patients with CAD. Despite the advent of drug-eluting stents, restenosis remains the main challenge in treating patients with CAD. In-stent restenosis (ISR) indicates the reduction in lumen diameter after percutaneous coronary intervention, in which the vessel’s lumen re-narrowing is attributed to the aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) and dysregulation of endothelial cells (ECs). Increasing evidence has demonstrated that epigenetics is involved in the occurrence and progression of ISR. In this review, we provide the latest and comprehensive analysis of three separate but related epigenetic mechanisms regulating ISR, namely, DNA methylation, histone modification, and non-coding RNAs. Initially, we discuss the mechanism of restenosis. Furthermore, we discuss the biological mechanism underlying the diverse epigenetic modifications modulating gene expression and functions of VSMCs, as well as ECs in ISR. Finally, we discuss potential therapeutic targets of the small molecule inhibitors of cardiovascular epigenetic factors. A more detailed understanding of epigenetic regulation is essential for elucidating this complex biological process, which will assist in developing and improving ISR therapy.

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The Regulatory Roles of Non-coding RNAs in Angiogenesis and Neovascularization From an Epigenetic Perspective

Cited by 35 publications

References 169 publications

CircATRNL1 activates Smad4 signaling to inhibit angiogenesis and ovarian cancer metastasis via miR‐378

CircATRNL1 activates Smad4 signaling to inhibit angiogenesis and ovarian cancer metastasis via miR‐378

Epigenetic Regulation of Dental Pulp Stem Cell Fate

Targeting the epigenome in in-stent restenosis: from mechanisms to therapy

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