Effects of all-trans retinoic acid on VEGF and HIF-1α expression in glioma cells under normoxia and hypoxia and its anti-angiogenic effect in an intracerebral glioma model

Chen, Liang; Guo, Shiwen; Yang, Lifen

doi:10.3892/mmr.2014.2543

Cited by 24 publications

(19 citation statements)

References 35 publications

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“…9). RA has been shown to upregulate expression of VEGF-A in several cell culture model systems (Liang et al, 2013, 2014; Wu et al, 2011). RA stimulates signaling in target cells through its receptors, RAR and RXR, which bind to DNA motifs known as retinoic acid response elements (RARE), in the promoter of the target genes (Ruberte et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…However, Vegfa promoter does not have a RARE sequence and thus RA may not act directly to regulate Vegfa transcription (Liang et al 2013). HIF1A is the most potent transcriptional regulator of VEGFA (Pagès and Pouysségur, 2005) and RA has been shown to up regulate HIF1A in several cell types (Fernández-Martínez et al, 2012; Fernández-Martínez et al, 2011; Liang et al, 2014) Also, RARE sequences have been identified in the HIF1A promoter (Fernandez-Martinez et al 2012). Future work will address the exact mechanism through which meningeal-derived RA regulates VEGF-A in the developing cerebral cortex.…”

Section: Discussionmentioning

confidence: 99%

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Cerebrovascular defects in Foxc1 mutants correlate with aberrant WNT and VEGF—A pathways downstream of retinoic acid from the meninges

Mishra

Choe

Pleasure

et al. 2016

Developmental Biology

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Growth and maturation of the cerebrovasculature is a vital event in neocortical development however mechanisms that control cerebrovascular development remain poorly understood. Mutations in or deletions that include the FOXC1 gene are associated with congenital cerebrovascular anomalies and increased stroke risk in patients. Foxc1 mutant mice display severe cerebrovascular hemorrhage at late gestational ages. While these data demonstrate Foxc1 is required for cerebrovascular development, its broad expression in the brain vasculature combined with Foxc1 mutant’s complex developmental defects have made it difficult to pinpoint its function(s). Using global and conditional Foxc1 mutants, we find 1) significant cerebrovascular growth defects precede cerebral hemorrhage and 2) expression of Foxc1 in neural crest-derived meninges and brain pericytes, though not endothelial cells, is required for normal cerebrovascular development. We provide evidence that reduced levels of meninges-derived retinoic acid (RA), caused by defects in meninges formation in Foxc1 mutants, is a major contributing factor to the cerebrovascular growth defects in Foxc1 mutants. We provide data that suggests that meninges-derived RA ensures adequate growth of the neocortical vasculature via regulating expression of WNT pathway proteins and neural progenitor derived-VEGF-A. Our findings offer the first evidence for a role of the meninges in brain vascular development and provide new insight into potential causes of cerebrovascular defects in patients with FOXC1 mutations.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cerebrovascular defects in Foxc1 mutants correlate with aberrant WNT and VEGF—A pathways downstream of retinoic acid from the meninges

Mishra

Choe

Pleasure

et al. 2016

Developmental Biology

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“…The present study showed that ATRA could induce the expression of Ang-2, and suppress the expression of Ang-1 and Tie-2, demonstrating that ATRA might play a role in preventing cartilage excessive vascularization in the antler growth. The notion was further confirmed in cancer cells (Kini et al 2001 ; Hoffmann et al 2007 ; Vourtsis et al 2013 ; Liang et al 2014 ). 9cRA also appears to have biological activity and has been used for treatment of Kaposi’s sarcoma and chronic hand eczema (Nelson et al 2013 ).…”

Section: Discussionmentioning

confidence: 85%

Expression and regulation of Angiopoietins and their receptor Tie-2 in sika deer antler

Zhang

Yue

Zhang

et al. 2017

Animal Cells and Systems

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The cartilage vascularization and chondrocyte survival are essential for endochondral ossification which occurs in the process of antler growth. Angiopoietins (Ang) is a family of major angiogenic growth factors and involved in regulating the vascularization. However, the expression and regulation of Angs in the antler are still unknown. The aim of this study is to localize the expression of Ang-1, Ang-2 and their receptor Tie-2 in sika deer antler using in situ hybridization and focused on analyzing the regulation of testosterone, estrogen, all-trans-retinoic acid (ATRA) and 9cRA on their expression in antler chondrocytes. The results showed that Ang-1, Ang-2 and Tie-2 were highly expressed in antler chondrocytes. Administration of testosterone to antler chondrocytes led to a notable increase in the expression of Ang-1 and Tie-2, and a reduction in the expression of Ang-2. The similar result was also observed after estrogen treatment. In contrast, ATRA and 9cRA could inhibit the expression of Ang-1 in antler chondrocytes and heighten the expression of Ang-2. Simultaneously, ATRA could downregulate the expression of Tie-2 in antler chondrocytes at 12 and 24 h, while 9cRA upregulate the expression of Tie-2 at 3 and 6 h. Collectively, Ang-1, Ang-2 and Tie-2 are expressed in antler chondrocytes and their expression can be affected by testosterone, estrogen, ATRA and 9cRA.

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“…28 – 30 Several studies have demonstrated that HIF1α functions as an oncogene in glioma. 31 – 33 High expression of HIF1α in glioma predicted a poor outcome. HIF1α increases autophagy and development of glioma through regulation of the miR-224-3p/ATG pathway.…”

Section: Discussionmentioning

confidence: 99%

<p>MiR-935/HIF1α Feedback Loop Inhibits the Proliferation and Invasiveness of Glioma</p>

Huang¹,

Chen²,

Liu³

et al. 2020

OTT

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Objective The biological functions and molecular mechanisms of miR-935 have been widely investigated in various types of cancer. The aim of the present study was to explore the function of miR-935 in glioma. Methods Bioinformatic analysis and quantitative real-time fluorescent PCR (qRT-PCR) were used to determine the expression of miR-935 in glioma tissues and glioma cell lines. Chi-square test was performed to analyze the relationship between the expression of miR-935 and clinical traits. CCK-8 assay, colony formation assay, cell cycle analysis and subcutaneous tumorigenesis model in nude mice were conducted to determine the effects of miR-935 on the proliferation of glioma cells both in vitro and in vivo. Wound healing and transwell assays were used to detect the effects of miR-935 on the migration and invasion of glioma cells in vitro. The relationship between miR-935 and HIF1α was analyzed using bioinformatics, luciferase reporter assay and Western blotting. Results The expression of miR-935 was lower in glioma tissues than in the adjacent tissues, and in cell lines than in the normal human astrocytes (NHAs), and the low expression levels of miR-935 predicted a poor outcome. Exogenous overexpression of miR-935 inhibited the proliferation of glioma cells both in vitro and in vivo, and suppressed the migration and invasion of glioma cells in vitro. HIF1α was identified as the target of miR-935, whereas miR-935 overexpression decreased the expression of HIF1α and its target genes VEGF , MCL1 and GLUT1 . Strikingly, overexpression of HIF1α significantly decreased the expression of miR-935, whereas silencing HIF1α increased the expression of miR-935. Similarly, HIF1α overexpression remarkably reversed the inhibitory effects of miR-935 on the proliferation, migration and invasion of glioma cells. Conclusion Overall, present study reveals the presence of miR-935/HIF1α feedback loop in glioma, which inhibits the development of glioma. This feedback loop may be a potential target for the treatment of glioma.

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Effects of all-trans retinoic acid on VEGF and HIF-1α expression in glioma cells under normoxia and hypoxia and its anti-angiogenic effect in an intracerebral glioma model

Cited by 24 publications

References 35 publications

Cerebrovascular defects in Foxc1 mutants correlate with aberrant WNT and VEGF—A pathways downstream of retinoic acid from the meninges

Cerebrovascular defects in Foxc1 mutants correlate with aberrant WNT and VEGF—A pathways downstream of retinoic acid from the meninges

Expression and regulation of Angiopoietins and their receptor Tie-2 in sika deer antler

<p>MiR-935/HIF1α Feedback Loop Inhibits the Proliferation and Invasiveness of Glioma</p>

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