Tumor cell-secreted angiogenin induces angiogenic activity of endothelial cells by suppressing miR-542-3p

He, Ting; Qi, Feifei; Jia, Lin; Wang, Shan; Wang, Qianqian; Song, Nan; Fu, Yan; Li, Lin; Luo, Yongzhang

doi:10.1016/j.canlet.2015.07.036

Cited by 41 publications

(30 citation statements)

References 53 publications

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“…Recently, increasing attention has been paid to the influence of miRNAs on endothelial cell function. miR-542-3p was found to inhibit angiogenesis of vascular endothelial cells both in vivo and in vitro (43). Moreover, miR-18a inhibited proliferation and migration of choroid endothelial cells (44).…”

Section: Discussionmentioning

confidence: 97%

SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153

Xue

Liu

et al. 2017

Oncology Reports

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Malignant glioma, the most common intracranial primary tumor, is characterized by increased angiogenesis. Accumulating evidence has shown that long non-coding RNAs (lncRNAs) play an important role in a variety of biological behaviors of tumors. However, the role of lncRNAs in the regulation of glioma vascular endothelial cell function remains to be investigated. To simulate the glioma microenvironment, we applied glioma conditioned medium (GCM) to human cerebral microvascular endothelial cells (hCMECs). In the present study, the lncRNA SNHG15 was found to be highly expressed in glioma vascular endothelial cells. Cell Counting Kit-8 (CCK-8), migration and tube formation assays demonstrated that knockdown of SNHG15 inhibited glioma vascular endothelial cell proliferation, migration and tube formation in vitro. Furthermore, knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42, which are known to promote angiogenesis. Bioinformatics software and dual-luciferase system analysis confirmed that SNHG15 affected endothelial cell function by targeting miR-153. Additionally, the present study showed that miR-153 targeted the 3'‑untranslated region of VEGFA and Cdc42 and downregulated their expression. In conclusion, knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42 by targeting miR-153, consequently suppressing glioma vascular endothelial cell proliferation, migration and tube formation. Therefore, SNHG15 and miR-153 are new potential therapeutic targets for anti-angiogenesis treatment of glioma.

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Section: Discussionmentioning

confidence: 97%

SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153

Xue

Liu

et al. 2017

Oncology Reports

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“…For example, tumour‐derived osteopontin reprograms normal fibroblasts to promote angiogenesis . Angiogenin secreted by breast tumour cells triggers angiogenic activity in endothelial cells . Vascular remodelling is considered to be one of the key events in metastasis development .…”

Section: Introductionmentioning

confidence: 99%

miR‐155 overexpression is followed by downregulation of its target gene, NFE2L2, and altered pattern of VEGFA expression in the liver of melanoma B16‐bearing mice at the premetastatic stage

Aksenenko

Palkina

Сергеева

et al. 2019

Int J Experimental Path

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Summary MicroRNAs are involved in the control of tumour progression and in metastatic cascade dynamics. However, the role of microRNAs in distant organ reorganization at the premetastatic stage is less clear, although the process of premetastatic niche formation is a crucial event according to modern concepts of tumour dissemination. The role of the present study was to investigate the expression levels of miR‐155, miR‐21, miR‐205 and miR‐let7b, as well as that of their target genes, in target organs of melanoma metastasis at the premetastatic stage. The expression levels of both the pro‐oncogenic miR‐155 and the tumour suppressive miR‐205 were found to be altered in the premetastatic liver of melanoma B16‐bearing mice. Bioinformatics analysis identified the target genes of miR‐155 to be nuclear factor, erythroid 2 like 2 (NFE2L2), secretogranin II, miR‐205, semaphorin 5A and vascular endothelial growth factor A (VEGFA). Among those, the redox status regulatory factor NFE2L2 was downregulated, which corresponded to increased levels of miR‐155. Due to the ability of pro‐oxidative events to initiate angiogenesis, VEGFA levels were evaluated in the premetastatic liver by immunohistochemistry, which revealed increased VEGFA expression in the central parts of the organ and diminished expression in the periphery. Taken together, these findings may support the concept of functional organ reorganization due to melanoma progression.

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“…miR-542-3p was found to inhibit angiogenesis of vascular endothelial cells both in vivo and in vitro. 46 Moreover, miR-18a inhibited proliferation and migration of choroid endothelial cells. 47 Our study showed that overexpression of miR-186 inhibited proliferation, migration, and in vitro tube formation of glioma vascular endothelial cells, suggesting that miR-186 could become a potential target for glioma anti-angiogenic therapy.…”

Section: Discussionmentioning

confidence: 99%

PVT1 affects growth of glioma microvascular endothelial cells by negatively regulating miR-186

Wang

Xue

et al. 2017

Tumour Biol.

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Vigorous angiogenesis is one of the reasons for the poor prognosis of glioma. A number of studies have shown that long non-coding RNA can affect a variety of biological behaviors of tumors. However, the influence of long non-coding RNAs on glioma vascular endothelial cells remains unclear. To simulate the glioma microenvironment, we applied glioma-conditioned medium to human cerebral microvascular endothelial cells. The long non-coding RNA PVT1 was found to be highly expressed in glioma vascular endothelial cells. Cell Counting Kit-8, migration, and tube formation assays showed that PVT1 overexpression promoted glioma vascular endothelial cells proliferation, migration, and angiogenesis. We also found that PVT1 overexpression upregulated the expression of the autophagy-related proteins Atg7 and Beclin1, which induced protective autophagy. Bioinformatics software and dual-luciferase system analysis confirmed that PVT1 acts by targeting miR-186. In addition, our study showed that miR-186 could target the 3′ untranslated region of Atg7 and Beclin1 to decrease their expression levels, thereby inhibiting glioma-conditioned human cerebral microvascular endothelial cell autophagy. In conclusion, PVT1 overexpression increased the expression of Atg7 and Beclin1 by targeting miR-186, which induced protective autophagy, thus promoting glioma vascular endothelial cell proliferation, migration, and angiogenesis. Therefore, PVT1 and miR-186 can provide new therapeutic targets for future anti-angiogenic treatment of glioma.

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Tumor cell-secreted angiogenin induces angiogenic activity of endothelial cells by suppressing miR-542-3p

Cited by 41 publications

References 53 publications

SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153

SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153

miR‐155 overexpression is followed by downregulation of its target gene, NFE2L2, and altered pattern of VEGFA expression in the liver of melanoma B16‐bearing mice at the premetastatic stage

PVT1 affects growth of glioma microvascular endothelial cells by negatively regulating miR-186

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