OVA66 promotes tumour angiogenesis and progression through enhancing autocrine VEGF-VEGFR2 signalling

Song, Feifei; Chen, Qi; Rao, Wei; Zhang, Renfeng; Wang, Ying; Ge, Heng; Wei, Qing

doi:10.1016/j.ebiom.2019.02.051

Cited by 27 publications

(27 citation statements)

References 25 publications

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“…Accordingly, in our study, we also found that silencing VEGF in NPC cells led to a decrease in N-cadherin, vimentin and MMPs and increase in E-cadherin, suggesting that VEGF can affect metastasis via EMT and MMPs in NPC cells. Emerging findings have demonstrated that autocrine VEGF-VEGFR2 signalling serves as an angiogenic modulator that controls tumorigenesis and malignant behaviour in many cancer cells, including ovarian cancer and skin epithelial cancer [11,[16][17][18]21]. In our study, we found that NPC cells secreted VEGF and promoted angiogenesis in a paracrine manner, further supporting the role of VEGF in tumour progression.…”

Section: Discussionsupporting

confidence: 80%

“…Emerging findings have demonstrated that autocrine VEGF-VEGFR2 signalling serves as an angiogenic modulator that controls tumorigenesis and malignant behaviour in many cancer cells, including ovarian cancer and skin epithelial cancer 11 , 16 - 18 , 21 . In our study, we found that NPC cells secreted VEGF and promoted angiogenesis in a paracrine manner, further supporting the role of VEGF in tumour progression.…”

Section: Discussionmentioning

confidence: 99%

“…In the last decade, many studies have demonstrated that VEGF secreted by cancer cells stimulates cell proliferation and metastasis not only in a paracrine manner but also via the autocrine activation of VEGF receptors (VEGFR1/2/3) [11][12][13][14][15][16][17][18]. The binding of VEGF to VEGFR2 is the key step in tumour angiogenesis [12,19], and autocrine VEGF-VEGFR2 signalling promotes tumour progression and migration [16,20,21]. The matrix metalloproteinase (MMP) family plays an important role in the process of tumour metastasis.…”

Section: Ivyspring International Publishermentioning

confidence: 99%

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VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma

et al. 2020

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Background: Vascular endothelial growth factor (VEGF) is an important pro-angiogenic factor. Accumulating data have indicated that VEGF is involved in tumour metastasis. However, the mechanism through which VEGF regulates nasopharyngeal carcinoma (NPC) metastasis is largely unknown. This study aimed to examine the biological function of VEGF in NPC metastasis and its underlying mechanism. Methods: We used western blotting and qPCR to examine the difference in VEGF expression between NPC cells and the immortalized nasopharyngeal epithelial cell line NP69. Wound healing assays, transwell assays and animal experiments were used to further verify the role of VEGF in the invasion and migration of NPC cells. The protein levels of the epithelial-mesenchymal transition (EMT) and matrix metalloproteinase (MMP) family were analysed by immunofluorescence (IF) and western blotting. Enzyme-linked immunosorbent assay (ELISA) and transwell assays were used to determine whether VEGF enhanced the invasion and migration of NPC cells in an autocrine manner. Western blotting was used to examine how autocrine VEGF-VEGFR2 signalling regulated EMT and MMPs. Results: We observed higher levels of VEGF in NPC cells than that in NP69 cells and identified an association between high VEGF levels and tumour invasion and migration. Mechanistically, the VEGF-mediated increase in EMT markers, MMP2 and MMP9 promoted NPC cell invasion and migration. Additionally, NPC cells secreted VEGF to promote cell invasion, migration and angiogenesis. Autocrine VEGF-VEGFR2 signalling increased ERK1/2 phosphorylation, promoted EMT process and MMPs at the indicated times. Conclusion: This study revealed that VEGF plays a role in controlling NPC cell metastasis by regulating EMT markers and MMPs in an autocrine manner.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Ivyspring International Publishermentioning

confidence: 99%

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VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma

et al. 2020

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“…In cancer, angiogenesis involves interaction between tumor cells, endothelial cells, and mesenchymal cells, which is orchestrated by growth factors or cytokines and their corresponding receptors. Among them, VEGFA plays a key role in the process of angiogenesis . Recent studies have shown that a variety of cancer cells can upregulate the expression of VEGFA, thereby promoting tumor‐induced angiogenesis .…”

Section: Discussionmentioning

confidence: 99%

RPV‐modified epirubicin and dioscin co‐delivery liposomes suppress non‐small cell lung cancer growth by limiting nutrition supply

et al. 2020

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| 621 wileyonlinelibrary.com/journal/cas | INTRODUC TI ONLung cancer is one of the most common malignancies and a leading cause of cancer-related death worldwide. 1 Among all lung cancers, approximately 85% are non-small cell lung cancer (NSCLC), for which morbidity is significantly higher than for small cell lung cancer. 2 In the past decade, targeted therapy, immunotherapy, and similar approaches rapidly developed to become the new treatment modalities for NSCLC. Despite recent developments and improvements in diagnosis and treatment, prospects for patients with NSCLC are dismal and the 5-year overall survival rate is only 15%-18%. 3,4 Rapid growth and metastasis are basic biological characteristics of malignant tumors, including NSCLC. 5 It is well known that angiogenesis plays a key role in cancer growth and metastasis. Anti-angiogenesis treatment has evolved to achieve encouraging results, but despite the widespread application of anti-angiogenic drugs, they have not attained satisfactory efficacy. [6][7][8] This means that alternative nutrient supply channels support tumor growth.Vasculogenic mimicry (VM) is defined as formation of vascu- lar-like structures lined with tumor cells without the presenceThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractChemotherapy for non-small cell lung cancer (NSCLC) is far from satisfactory, mainly due to poor targeting of antitumor drugs and self-adaptations of the tumors.Angiogenesis, vasculogenic mimicry (VM) channels, migration, and invasion are the main ways for tumors to obtain nutrition. Herein, RPV-modified epirubicin and dioscin co-delivery liposomes were successfully prepared. These liposomes showed ideal physicochemical properties, enhanced tumor targeting and accumulation in tumor sites, and inhibited VM channel formation, tumor angiogenesis, migration and invasion. The liposomes also downregulated VM-related and angiogenesis-related proteins in vitro. Furthermore, when tested in vivo, the targeted co-delivery liposomes increased selective accumulation of drugs in tumor sites and showed extended stability in blood circulation. In conclusion, RPV-modified epirubicin and dioscin co-delivery liposomes showed strong antitumor efficacy in vivo and could thus be considered a promising strategy for NSCLC treatment. K E Y W O R D Sangiogenesis, cell-penetrating peptide, co-delivery liposome, non-small cell lung cancer, vasculogenic mimicry

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“…Besides, it is reported that NudCD1 promotes proliferation, migration, and invasion of renal carcinoma cells [11]. Additionally, NudCD1 promotes tumor angiogenesis and progression through enhancing autocrine VEGF-VEGFR2 signaling [12]. NudCD1 affects the progression of renal cell carcinoma through regulating the LIS1/dynein signaling pathway [13].…”

Section: Introductionmentioning

confidence: 99%

NudCD1 Promotes the Proliferation and Metastasis of Non-Small Cell Lung Cancer Cells through the Activation of IGF1R-ERK1/2

Xia

Zhang³

2020

Pathobiology

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Background: NudC domain containing 1 (NudCD1) is an oncoprotein related to diverse cancers. This study aims to investigate the expression, role, and regulatory mechanism of NudCD1 in non-small cell lung cancer (NSCLC). Methods: qRT-PCR, Western blot, and immunohistochemistry were performed to detect the expressions of NudCD1 in NSCLC tissues and cell lines. The correlation between NudCD1 expression and clinical features was determined by the χ 2 test. Besides, shRNA was used to construct the NudCD1 low expression model of NCI-H1299 and NCI-H460 cells, and CCK-8 and transwell assay were conducted to monitor the changes of proliferation, migration, and invasion of cancer cells. The expression levels of epithelial-mesenchymal transition markers and IGF1R-ERK1/2 signaling pathway proteins were detected by Western blot. Results: The expression of NudCD1 in NSCLC was higher than that in normal tissues, and the increased expression of NudCD1 was significantly correlated with increased T stage and lymph node metastasis. Moreover, patients with high expression of NudCD1 had worse prognosis. NudCD1 knockdown was proven to impede the proliferation but facilitate the migration and invasion of cancer cells. Furthermore, knockdown of NudCD1 resulted in an increase in the expression of E-cadherin and a decrease in the expression of vimentin. We also observed that NudCD1 overexpression promoted the phosphorylation of IGF1R and ERK1/2 proteins. Conclusion: NudCD1 promotes the proliferation and metastasis of NSCLC cells via activation of IGF1R-ERK1/2, which indicates that NudCD1 may be a potential therapy target of NSCLC.

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OVA66 promotes tumour angiogenesis and progression through enhancing autocrine VEGF-VEGFR2 signalling

Cited by 27 publications

References 25 publications

VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma

VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma

RPV‐modified epirubicin and dioscin co‐delivery liposomes suppress non‐small cell lung cancer growth by limiting nutrition supply

NudCD1 Promotes the Proliferation and Metastasis of Non-Small Cell Lung Cancer Cells through the Activation of IGF1R-ERK1/2

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