Vascular Endothelial Growth Inhibitor, a Cytokine of the Tumor Necrosis Factor Family, is Associated With Epithelial-Mesenchymal Transition in Renal Cell Carcinoma

Zhao, Qiang; Liu, Tiezhu; Hong, Bo; Wang, Feng; Zhou, Changhua; Du, Xin; Chen, Siqi; Deng, Xiaohu; Duoerkun, Shayiremu; Li, Qing; Yang, Yong; Gong, Kan; Zhang, Ning

doi:10.1097/pai.0000000000000517

Cited by 8 publications

(8 citation statements)

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“…In addition, Chew et al (14) demonstrated that overexpression of VEGI abrogates xenograft tumour progression by reducing tumour growth rate and microvessel density. It has also been demonstrated that overexpression of VEGI inhibits RCC cell motility, EMT, vascular endothelial tube formation and tumour growth (21)(22)(23)(24). Furthermore, VEGI participates in regulating the biological functions of several tumour cell lines, including breast carcinoma (MCF-7), cervical carcinoma (HeLa) and myeloid tumour (U-937 and ML-1a) cell lines (34,35).…”

Section: Discussionmentioning

confidence: 99%

“…VEGI is highly expressed in kidney, bladder, prostate, lung, breast and colon tissues (16)(17)(18)(19)(20)(21). Our previous studies revealed that overexpression of VEGI174 significantly inhibited RCC cell proliferation, motility, adhesion and epithelial-mesenchymal transition (EMT) in vitro and in vivo (21)(22)(23)(24). Taken together, these previous data suggested that VEGI174 exerts inhibitory effects on RCC; therefore, it may be valuable to be further study VEGI174 with regards to RCC treatment.…”

Section: Introductionmentioning

confidence: 99%

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VEGI174 protein and its functional domain peptides exert antitumour effects on renal cell carcinoma

et al. 2018

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Vascular endothelial growth inhibitor (VEGI) has been identified as an anti-angiogenic cytokine. However, the effects of VEGI174 protein, and its functional domain peptides V7 and V8, on renal cell carcinoma (RCC) remain unknown. In the present study, the protein and peptides were biosynthesised as experimental agents. The A498 and 786-O RCC cell lines, and an established mouse xenograft model, were separately treated with VEGI174, V7 or V8. Cellular functions, including proliferation, migration and invasion, were subsequently detected. Cell migration and invasion were monitored using the xCELLigence system. Furthermore, tumour growth and mouse behaviours, including mobility, appetite and body weight, were assessed. The results demonstrated that VEGI174, V7 and V8 inhibited the proliferation, migration and invasion of A498 and 786-O cell lines when administered at concentrations of 1 and 100 pM, 10 nM and 1 µM. The inhibitory effects exhibited dose-and time-dependent antitumour activity. Furthermore, VEGI174, V7 and V8 inhibited tumour growth in A498 and 786-O xenograft mice. In the A498 xenografts, the tumour growth inhibition (TGI) rates in the VEGI174-, V7-and V8-treated groups were 71, 20 and 31%, respectively. In the 786-O xenografts, the TGI rates in the VEGI174-, V7-and V8-treated groups were 34, 26 and 31%, respectively. There was no significant loss in body weight and no cases of mortality were observed for all treated mice. In conclusion, VEGI174, V7 and V8 exhibited potential antitumour effects and were well tolerated in vivo. V7 and V8, as functional domain peptides of the VEGI174 protein, may be studied for the future treatment of RCC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

VEGI174 protein and its functional domain peptides exert antitumour effects on renal cell carcinoma

et al. 2018

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“…In human cancers, higher expression of VEGI - 192 mRNA was found in early stages of clear-cell renal cell carcinoma (ccRCC) than in advanced stages of ccRCC. Furthermore, VEGI - 192 mRNA levels were negatively correlated with tumor histological differentiation grade [ 12 ] and epithelial–mesenchymal transition in renal tumor [ 13 ]. In human pituitary tumors, high levels of VEGI - 192 mRNA were associated with lower tumor grade and invading pituitary tumors were characterized by lower VEGI - 192 mRNA expression [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Distinct Expression Patterns of Two Tumor Necrosis Factor Superfamily Member 15 Gene Isoforms in Human Colon Cancer

et al. 2019

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Background Tumor necrosis factor superfamily member 15 ( TNFSF15 ) gene is involved in development of several cancers. It encodes two proteins: tumor necrosis factor ligand-related molecule 1A (TL1A) and vascular endothelial growth inhibitor 192 (VEGI-192). The main receptor for TL1A is death receptor 3 (DR3). Aims We investigated expression of TL1A, VEGI - 192, and DR3 transcripts in different stages of colon cancer and compared them with survival of patients. We also aimed to reveal possible effects of microsatellite instability (MSI) and selected TNFSF15 single-nucleotide polymorphisms (SNPs) on expression of this gene. Methods Forty-five healthy individuals and 95 colon cancer patients were included in the study. Expression of VEGI - 192, TL1A, and DR3 was measured by quantitative PCR. SNP and MSI analyses were performed on DNA isolated from normal or cancer tissue. Results Expression of VEGI - 192 and TL1A was elevated in colon cancer, although the level of VEGI - 192 decreased, while the level of TL1A increased with the progression of cancer. Patients with low expression of TL1A and/or high expression of VEGI - 192 in tumor-transformed tissue showed longer survival. DR3 expression was decreased in the cancer, but it did not change with the tumor progression. Alleles T of rs6478108 and G of rs6478109 SNPs were associated with elevated expression of the TNFSF15 gene. There was no relation between the MSI status and TNFSF15 expression levels. Conclusions Expression of the TNFSF15 gene isoforms was associated with the progression of colon cancer. Levels of TL1A and VEGI - 192 transcripts can be considered as independent prognostic factors for colon cancer.

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“…In addition to those developmental events in which EMT plays a fundamental role, EMT is also determinant in several pathophysiological conditions, in particular in cancer. Multiple sets of evidence demonstrate that EMT is involved in oncogenic processes of different tissues such as in the gonads in the development of ovarian surface epithelial cancer [ 62 , 63 , 64 , 65 ], in the kidney in clear cell renal cell carcinoma [ 66 , 67 , 68 , 69 , 70 ], in the lungs leading to both adenocarcinoma and non-small cellular lung cancer (NSCLC) [ 71 , 72 , 73 , 74 , 75 ], in the liver in cholangiocarcinoma and hepatocellular carcinoma [ 76 , 77 , 78 , 79 ], and in the pancreas [ 80 , 81 , 82 , 83 ] as well as in other tissues [ 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 ].…”

Section: Introductionmentioning

confidence: 99%

Functional Role of Non-Coding RNAs during Epithelial-To-Mesenchymal Transition

Expósito-Villén

Aránega

Franco

2018

ncRNA

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Epithelial-to-mesenchymal transition (EMT) is a key biological process involved in a multitude of developmental and pathological events. It is characterized by the progressive loss of cell-to-cell contacts and actin cytoskeletal rearrangements, leading to filopodia formation and the progressive up-regulation of a mesenchymal gene expression pattern enabling cell migration. Epithelial-to-mesenchymal transition is already observed in early embryonic stages such as gastrulation, when the epiblast undergoes an EMT process and therefore leads to the formation of the third embryonic layer, the mesoderm. Epithelial-to-mesenchymal transition is pivotal in multiple embryonic processes, such as for example during cardiovascular system development, as valve primordia are formed and the cardiac jelly is progressively invaded by endocardium-derived mesenchyme or as the external cardiac cell layer is established, i.e., the epicardium and cells detached migrate into the embryonic myocardial to form the cardiac fibrous skeleton and the coronary vasculature. Strikingly, the most important biological event in which EMT is pivotal is cancer development and metastasis. Over the last years, understanding of the transcriptional regulatory networks involved in EMT has greatly advanced. Several transcriptional factors such as Snail, Slug, Twist, Zeb1 and Zeb2 have been reported to play fundamental roles in EMT, leading in most cases to transcriptional repression of cell–cell interacting proteins such as ZO-1 and cadherins and activation of cytoskeletal markers such as vimentin. In recent years, a fundamental role for non-coding RNAs, particularly microRNAs and more recently long non-coding RNAs, has been identified in normal tissue development and homeostasis as well as in several oncogenic processes. In this study, we will provide a state-of-the-art review of the functional roles of non-coding RNAs, particularly microRNAs, in epithelial-to-mesenchymal transition in both developmental and pathological EMT.

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Vascular Endothelial Growth Inhibitor, a Cytokine of the Tumor Necrosis Factor Family, is Associated With Epithelial-Mesenchymal Transition in Renal Cell Carcinoma

Cited by 8 publications

References 31 publications

VEGI174 protein and its functional domain peptides exert antitumour effects on renal cell carcinoma

VEGI174 protein and its functional domain peptides exert antitumour effects on renal cell carcinoma

Distinct Expression Patterns of Two Tumor Necrosis Factor Superfamily Member 15 Gene Isoforms in Human Colon Cancer

Functional Role of Non-Coding RNAs during Epithelial-To-Mesenchymal Transition

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