Retraction Note To: VEGF Silencing Inhibits Human Osteosarcoma Angiogenesis and Promotes Cell Apoptosis via PI3K/AKT Signaling Pathway

Zhao, Jian; Zhang, Ziru; Zhao, Na; Ma, Baoan; Fan, Qingyu

doi:10.1007/s12013-017-0794-5

Cited by 14 publications

(17 citation statements)

References 27 publications

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“…Thus, the gene is a potential therapeutic target in various human solid tumors 26 , 43 . VEGF is a downstream protein of the JAK2/STAT3 signaling pathways that plays a pivotal role in angiogenesis 45 , 46 . VEGF is usually upregulated in multiple cancers, including OS 46 .…”

Section: Discussionmentioning

confidence: 99%

“…VEGF is a downstream protein of the JAK2/STAT3 signaling pathways that plays a pivotal role in angiogenesis 45 , 46 . VEGF is usually upregulated in multiple cancers, including OS 46 . To investigate whether the suppression or inactivation of this pathway is inherently associated with the PARK2 gene, the stably overexpressed PARK2 cell lines were used.…”

Section: Discussionmentioning

confidence: 99%

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PARK2 inhibits osteosarcoma cell growth through the JAK2/STAT3/VEGF signaling pathway

et al. 2018

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Osteosarcoma (OS) is the most common primary malignant bone tumor mainly occurring in children and adolescents. In past decades, studies revealed that PARK2 was a vital tumor suppressor gene in many malignant solid tumors. However, the role of PARK2 in OS remains largely unclear. Therefore, we assessed PARK2 expression in OS tissue and adjacent non-tumor tissues by immunohistochemical (IHC) analysis, and evaluated PARK2 mRNA expression in OS cell lines by real-time PCR analysis. The HOS and U2OS cell lines were employed to establish a PARK2 overexpression model. Using this model, we investigated the potential role of PARK2 in OS and explored the underlying molecular mechanisms. Our study showed PARK2 was downregulated in OS tissue and cell lines, which was significantly associated with higher tumor stage (P < 0.05). Overexpression of PARK2 arrested the cell cycle, inhibited cell proliferation, migration, and invasion, induced cell apoptosis, and reduced tube formation in vitro. Moreover, overexpression of PARK2 significantly suppressed tumor growth and angiogenesis in vivo. Additionally, PARK2 negatively regulated OS development through the JAK2/STAT3/VEGF pathway. Our findings demonstrate that PARK2 is a tumor suppressor gene that may negatively affect OS growth and angiogenesis via partly inhibiting the JAK2/STAT3/VEGF signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

PARK2 inhibits osteosarcoma cell growth through the JAK2/STAT3/VEGF signaling pathway

et al. 2018

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“…The down-regulation of VEGF is a key to the mechanisms underlying the inhibition of the development and progression of endometrial carcinoma [12]. Silencing VEGF has inhibited cell proliferation and angiogenesis in human osteosarcoma [13] and also suppressed the occurrence of lung cancer [14]. Other evidence suggests that the expression of VEGF is regulated by its methylation, hypermethylation of VEGF caused a decrease in the expression of mRNA [15,16].…”

Section: Introductionmentioning

confidence: 99%

miR-148a-3p inhibits DNMT1-mediated methylation of VEGF and promotes proliferation and invasion in glioma cells via the PI3K/Akt/eNOS signaling pathway

Huo

Chen

2020

Preprint

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Background: Abnormal DNA methylation in the promoter region of vascular endothelial growth factor (VEGF) has been observed in multiple types of cancer. Increasing evidence shows that miR-148a-3p is involved in the regulation of methylation. However, it is unclear how miR-148a-3p regulates VEGF methylation.Methods: Methylation-specific polymerase chain reaction (MSP) and bisulfate-sequencing PCR (BSP) were performed to detect the methylation level of the VEGF promoter region in glioma tissues and cell lines. Then, we used RT-qPCR to detect the expression of miR-148a-3p and VEGF in glioma tissues and cell lines. Human glioma U87 cells were transfected with miR-148a-3p mimic or a pcDNA3.1 overexpression vector of VEGF, and then, the proliferation, invasion and apoptosis of U87 cells were examined with cell counting kit-8 (CCK-8), Transwell assay and Flow cytometry, respectively. We next examined the relationship between DNA methyltransferase 1 (DNMT1) and miR-148a-3p with online prediction and luciferase reporter gene experiments. Furthermore, we also used Western blotting to detect the protein levels of VEGF, DNMT1, PI3K, Akt and eNOS.Results: Both miR-148a-3p and VEGF were significantly up-regulated, and the promoter methylation of VEGF was hypomethylation in glioma. Overexpression miR-148a-3p or VEGF promoted the proliferation and invasion of U87 cells and inhibited the apoptosis. Silencing VEGF inhibited U87 cells proliferation and invasion and induced the apoptosis. Furthermore, miR-148a-3p regulated DNMT1 at the post-transcriptional. Overexpression of DNMT1 mediated an increase in the methylation level of VEGF, which reduced the expression of VEGF in U87 cells. The opposite was exact when DNMT1 was silenced. We also observed that silencing VEGF inhibited the activation of the PI3K/Akt/eNOS pathway and induced U87 cell apoptosis.Conclusion: These results indicated that miR-148a-3p down-regulates VEGF methylation by targeting DNMT1 and promotes the proliferation, invasion of the glioma cell through the PI3K/Akt/eNOS pathway.

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“…Currently, it has been reported that VEGFA is highly expressed in OS cells and strongly associated with the poor prognosis of the patients [13]. Inhibition of VEGFA signaling suppressed OS growth, metastasis and angiogenesis [14][15][16], suggesting that VEGFA could be a novel therapeutic target for OS.…”

Section: Introductionmentioning

confidence: 99%

Tumor cell-targeted delivery of CRISPR/Cas9 by aptamer-functionalized lipopolymer for therapeutic genome editing of VEGFA in osteosarcoma

Liang

Wang³

et al. 2017

Biomaterials

173

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Retraction Note To: VEGF Silencing Inhibits Human Osteosarcoma Angiogenesis and Promotes Cell Apoptosis via PI3K/AKT Signaling Pathway

Cited by 14 publications

References 27 publications

PARK2 inhibits osteosarcoma cell growth through the JAK2/STAT3/VEGF signaling pathway

PARK2 inhibits osteosarcoma cell growth through the JAK2/STAT3/VEGF signaling pathway

miR-148a-3p inhibits DNMT1-mediated methylation of VEGF and promotes proliferation and invasion in glioma cells via the PI3K/Akt/eNOS signaling pathway

Tumor cell-targeted delivery of CRISPR/Cas9 by aptamer-functionalized lipopolymer for therapeutic genome editing of VEGFA in osteosarcoma

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