MiR-23a targets RUNX2 and suppresses ginsenoside Rg1-induced angiogenesis in endothelial cells

Wu, Xiaodong; Guo, Tao; Liu, Li; Wang, Chao; Zhang, Kun; Liu, Hanqiang; Wang, Rui; Bai, Wen-Dong; Zhang, Mengyao

doi:10.18632/oncotarget.19489

Cited by 19 publications

(11 citation statements)

References 39 publications

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“…New research has found that lyophilized PRF can mediate Runx2enhanced craniofacial bone regeneration (Li et al, 2014). Furthermore, Rg1 can stimulate human umbilical vein endothelial cells to undergo angiogenesis via the miR-23a/ RUNX2/VEGF-A pathway (Wu et al, 2017). Therefore, key factors, such as the presence of bone tissue components in the "adipose tissue block" induced by PRF and Rg1 and the correlation between Runx2 expression in transplanted adipose stem cells and tumor formation, must be clarified before clinical trials.…”

Section: Rg1 Regulates the Proliferation And Differentiation Of Mscsmentioning

confidence: 99%

Ginsenoside Rg1 as an Effective Regulator of Mesenchymal Stem Cells

Liu

et al. 2020

Front. Pharmacol.

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Recently, breakthroughs have been made in the use of mesenchymal stem cells (MSCs) to treat various diseases. Several stem cell types have been authorized as drugs by the European Medicines Agency and the U.S. Food and Drug Administration. The Chinese official document "Notification of the management of stem cell clinical research (trial)" was also published in August 2015. Currently, China has approved 106 official stem cell clinical research filing agencies and 62 clinical research projects, which are mostly focused on MSC therapy. Hence, the optimization and development of stem cell drugs is imperative. During this process, maximizing MSC expansion, minimizing cell loss during MSC transplantation, improving the homing rate, precisely regulating the differentiation of MSCs, and reducing MSC senescence and apoptosis are major issues in MSC preclinical research. Similar to artemisinin extracted from the stems and leaves of Artemisia annua, ginsenoside Rg1 (Rg1) is purified from the root or stem of ginseng. In the human body, Rg1 regulates organ function, which is inseparable from its regulation of adult stem cells. Rg1 treatment may effectively regulate the proliferation, differentiation, senescence, and apoptosis of MSCs in different microenvironments in vitro or in vivo. In this review, we discuss recent advances in understanding the effect of Rg1 on MSCs and describe the issues that must be addressed and prospects regarding Rg1 regulation of MSCs in preclinical or clinical studies.

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Section: Rg1 Regulates the Proliferation And Differentiation Of Mscsmentioning

confidence: 99%

Ginsenoside Rg1 as an Effective Regulator of Mesenchymal Stem Cells

Liu

et al. 2020

Front. Pharmacol.

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“…Reduced TSGA10 expression led to the growth, migration, and tube formation of the vascular endothelial cells [50]. Wu et al showed that miR-23a might also suppress the expression of the vascular endothelial growth factor A (VEGF-A), by targeting its translational facilitator RUNX2 in the vascular endothelial cells [116].…”

Section: Biological Role Of the Mir-23a In Human Cancermentioning

confidence: 99%

microRNA-23a in Human Cancer: Its Roles, Mechanisms and Therapeutic Relevance

Wang

Tan

Feng

et al. 2018

Cancers

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microRNA-23a (miR-23a) is one of the most extensively studied miRNAs in different types of human cancer, and plays various roles in the initiation, progression, and treatment of tumors. Here, we comprehensively summarize and discuss the recent findings about the role of miR-23a in cancer. The differential expression of tissue miR-23a was reported, potentially indicating cancer stages, angiogenesis, and metastasis. miR-23a in human biofluid, such as plasma and salivary fluid, may be a sensitive and specific marker for early diagnosis of cancer. Tissue and circulating miR-23a serves as a prognostic factor for cancer patient survival, as well as a predictive factor for response to anti-tumor treatment. The direct and indirect regulation of miR-23a on multiple gene expression and signaling transduction mediates carcinogenesis, tumor proliferation, survival, cell migration and invasion, as well as the response to anti-tumor treatment. Tumor cell-derived miR-23a regulates the microenvironment of human cancer through manipulating both immune function and tumor vascular development. Several transcriptional and epigenetic factors may contribute to the dysregulation of miR-23a in cancer. This evidence highlights the essential role of miR-23a in the application of cancer diagnosis, prognosis, and treatment.

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“…MicroRNAs (miRNAs) are a group of single‐strand noncoding RNAs with around 23 nucleotides, reputed to bring about posttranscriptional inhibition on gene expression by targeting the 3′‐untranslated regions (3′UTRs) of mRNAs . Dysregulation of miRNAs could lead to diverse disorders such as cancer, and the oncogenic or tumor suppressive roles of miRNAs vary according to the type of mRNAs they target . miR‐488‐3p has been newly discovered to be a tumor suppressor in several cancers, such as in glioma, and melanoma .…”

Section: Introductionmentioning

confidence: 99%

“…8,9 Dysregulation of miRNAs could lead to diverse disorders such as cancer, and the oncogenic or tumor suppressive roles of miRNAs vary according to the type of mRNAs they target. [10][11][12][13][14] miR-488-3p has been newly discovered to be a tumor suppressor in several cancers, such as in glioma, 15 and melanoma. 16 However, never has the role of miR-488-3p been explored in ESCC.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐488‐3p inhibits proliferation and induces apoptosis by targeting ZBTB2 in esophageal squamous cell carcinoma

Yang

et al. 2019

J of Cellular Biochemistry

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Esophageal squamous cell carcinoma (ESCC) is the eighth most prevalent cancer and the sixth leading cause for cancer‐associated mortality. MicroRNAs (miRNAs) are increasingly reported to exert important regulatory functions in human cancers by regulating certain gene expression. miR‐488‐3p has been identified to be a tumor suppressor in multiple cancers, but its role in ESCC is yet to be investigated. The present study aimed to uncover the biological role and modulatory mechanism of miR‐488‐3p in ESCC. We first revealed the downregulation of miR‐488‐3p in ESCC tissues and cell lines. Gain‐of‐function assays confirmed that miR‐488‐3p overexpression abrogated proliferation and accelerated apoptosis. Mechanistically, we identified via bioinformatics tool and confirmed that zinc finger and BTB domain containing 2 (ZBTB2) was a target for miR‐488‐3p. Moreover, miR‐488‐3p activated the p53 pathway through suppressing ZBTB2. Finally, rescue assays proved that ZBTB2 was involved in the regulation of miR‐488‐3p on proliferation and apoptosis in ESCC. Additionally, we verified that miR‐488‐3p had alternate targets in ESCC by confirming the involvement of protein kinase, DNA‐activated, catalytic subunit (PRKDC), a known target for miR‐488‐3p, in miR‐488‐3p‐mediated regulation on ESCC. In sum, this study revealed that miR‐488‐3p inhibited proliferation and induced apoptosis by targeting ZBTB2 and activating p53 pathway in esophageal squamous cell carcinoma, providing a novel biological target for ESCC.

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MiR-23a targets RUNX2 and suppresses ginsenoside Rg1-induced angiogenesis in endothelial cells

Cited by 19 publications

References 39 publications

Ginsenoside Rg1 as an Effective Regulator of Mesenchymal Stem Cells

Ginsenoside Rg1 as an Effective Regulator of Mesenchymal Stem Cells

microRNA-23a in Human Cancer: Its Roles, Mechanisms and Therapeutic Relevance

MicroRNA‐488‐3p inhibits proliferation and induces apoptosis by targeting ZBTB2 in esophageal squamous cell carcinoma

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