Relationship between tumour angiogenesis and expression of cyclo-oxygenase-2 and vascular endothelial growth factor-A in human renal cell carcinoma

Yang, Sheng; Gao, Qin; Jiang, Wei

doi:10.1177/0300060514545799

Cited by 7 publications

(7 citation statements)

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“…In many physiologic and pathologic processes, angiogenesis is the basis of chronic inflammation, ischemic disease and cancer. [ 28 ] It is a multistep process occurring in preexisting blood vessels, including newly blood vessels migration, extracellular matrix remodeling, and endothelial cell proliferation and migration. [ 29 30 ] The results of the present study, COX-2 and VEGF expression were decreased significantly after treated with OB [ Figure 4 ], it suggested that OB could play a potential role for treating liver cancer through the regulation of COX-2/VEGF signaling pathway, cutting off the blood supply a neoplastic lesion could be potentially starved into remission, then indirectly play antitumor effect.…”

Section: Discussionmentioning

confidence: 99%

Evidence for the involvement of COX-2/VEGF and PTEN/Pl3K/AKT pathway the mechanism of oroxin B treated liver cancer

Meng

Bao

et al. 2018

Phcog Mag

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Background:Oroxin B (OB) is one of flavonoids isolated from traditional Chinese herbal medicine Oroxylum indicum (L.) Vent. Recent studies suggest that flavonoids have obvious anti-liver tumors effect, but the precise molecular mechanism is still unclear.Objective:The current study was performed to investigate the antitumor effects of OB on human hepatoma cell line SMMC-772 and explore the part of molecular mechanisms in this process.Materials and Methods:MTT method, terminal deoxynucleotidyl transferase dUTP nick end labeling assay and flow cytometry were utilized to detect the inhibition of proliferation and the apoptosis after treating OB in of SMMC-7721 cells. The mRNA and proteins expressions of COX-2, vascular endothelial growth factor (VEGF), phosphatidylinositol-3-kinase (PI3K), p-AKT, and PTEN were measured by a real-time polymerase chain reaction and Western Blot method.Results:The results showed that OB inhibited proliferation of SMMC-7721 cell in a dose-dependent manner, and induced its apoptosis. Moreover, OB unregulated PTEN and downregulated COX-2, VEGF, p-AKT, and PI3K.Conclusion:Our results demonstrated that OB significantly inhibits proliferation and induce apoptosis, which may be strongly associated with the inhibiting COX-2/VEGF and PTEN/PI3K/AKT pathway signaling pathway in SMMC-7721 cells, OB potentially be used as a novel therapeutic agent for liver cancer.SUMMARY OB (Oroxin B) is one of the effective flavonoid components of traditional Chinese medicine O. indicum (L.)OB can inhibite the proliferation and promoted apoptosis of the human hepatoma cell line SMMC 7721OB plays a role of antitumor effect may to regulate COX 2/VEGF and PTEN/PI3K/AKT pathways directly or indirectly. Abbreviations used: OB: Oroxin B; MTT: 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide; COX-2: cyclooxygenase-2; PI3K: phosphatidylinositol 3 kinase; PTEN: Phosphatase and tensin homolog deleted on chromosome ten; VEGF: Vascular endothelial growth factor; RT-PCR: Reverse transcription polymerase chain reaction; DAPI: Diamidino 2 phenylindole; PBS: Phosphate buffer saline; FITC: Fluorescein isothiocyanate; PI: Propidium Iodide; RIPA: Radio immunoprecipitation assay lysis buffer; PMSF: Phenylmethanesulfonyl fluoride; PAGE: Polyacrylamide gel electrophoresis.

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Section: Discussionmentioning

confidence: 99%

Evidence for the involvement of COX-2/VEGF and PTEN/Pl3K/AKT pathway the mechanism of oroxin B treated liver cancer

Meng

Bao

et al. 2018

Phcog Mag

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“…One of the key aspects of the inflammatory process is the association of COX-2 with the formation of carcinogens, tumor progression and inhibition of apoptosis, angiogenesis, and metastatic processes ( 21 ). COX-2 is commonly upregulated in various types of human cancer, including RCC ( 22 - 24 ). In order to elucidate the mechanism of EMCL as an anticancer agent, the present study investigated whether COX-2 is important in the biological activity of EMCL and found that EMCL inhibited the expression of COX-2, and inhibited the viability, migration and colony formation of human RCC cells.…”

Section: Discussionmentioning

confidence: 99%

“…COX-2 regulates the formation of carcinogens, assists in tumor progression, and inhibits apoptosis, angiogenesis and the metastatic process ( 21 ). COX-2 is commonly unregulated in various types of human cancer, including RCC ( 22 – 24 ). In vitro , in vivo , observational and clinical data have demonstrated that selective COX-2 inhibitors are effective in preventing proliferation, angiogenesis and inflammation, and inducing apoptosis in human cancer cells ( 5 , 14 , 25 ).…”

Section: Introductionmentioning

confidence: 99%

Epoxymicheliolide, a novelguaiane-type sesquiterpene lactone, inhibits NF‑κB/COX‑2 signaling pathways by targeting leucine�281 and leucine�25 in IKKβ in renal cell carcinoma

Zhu

Zhao

et al. 2018

Int J Oncol

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Parthenolide (PTL) is a sesquiterpene lactone compound obtained from Tanacetum parthenium (feverfew) and inhibits the activation of nuclear factor (NF)-κB. Epoxymicheliolide (EMCL) is a compound which is structurally related to PTL; however, EMCL is more stable under acidic and alkaline conditions. As a biologically active molecule, the detailed mechanism by which EMCL inhibits tumor activity remains to be elucidated. The present study evaluated the effect of EMCL on renal cell carcinoma (RCC) cells and identified the underlying mechanisms. It was found that treatment with EMCL significantly inhibited the proliferation of RCC cells in vitro and increased the induction of apoptosis by activating the mitochondria- and caspase-dependent pathway. Simultaneously, EMCL suppressed cell invasion and metastasis by inhibiting epithelial-mesenchymal transition, as observed in a microfluidic chip assay. Furthermore, using immunofluorescence analysis, an electrophoretic mobility shift assay and a dual-luciferase reporter assay, it was shown that treatment with EMCL significantly suppressed the expression of cyclooxygenase-2 by inhibiting the translocation of NF-κB p50/p65 and the activity of NF-κB. Collectively, the results indicated that EMCL suppressed tumor growth by inhibiting the activation of NF-κB and suggested that EMCL may be a novel anticancer agent in the treatment of RCC.

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“…COX‐2 is an inducible enzyme that catalyzes arachidonic acid to prostaglandins during inflammatory and tumorigenic stages. Many studies have revealed that COX‐2 might be involved in angiogenesis . Recent clinical epidemiological studies have demonstrated the preventive effect of COX inhibitors on cancer .…”

Section: Discussionmentioning

confidence: 99%

Micro ribonucleic acid (RNA)‐101 inhibits cell proliferation and invasion of lung cancer by regulating cyclooxygenase‐2

Zhang

et al. 2015

Thoracic Cancer

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BackgroundMicro ribonucleic acid (miR-101) can regulate the expression of cyclooxygenase-2 (COX-2) and participate in the pathogenesis of malignant tumors. This study investigates the effects of miRNA-101 and COX-2 in lung cancer and the impact of miR-101 on the proliferation and invasion of human lung cancer A549 cell line.MethodsThe expression of miR-101 in 20 separate lung cancer tissues was detected by real time polymerase chain reaction; COX-2 expression was also detected. A549 cells were transfected with miR-101 or negative control oligonucleotide duplex mimic (miR-NC). In vivo tumorigenesis abilities were detected in localized human lung cancer xeno-transplant models in BALB/c nude mice.ResultsMiR-101 expression was significantly lower and the level of COX-2 significantly higher in lung cancer tissues than in adjacent parenchyma (2.918 ± 1.006 vs. 5.953 ± 1.976, P = 0.001; 0.887 ± 0.260 vs. 0.355 ± 0.156, P = 0.001, respectively). Correlation analysis revealed that miR-101 negatively correlated with COX-2 in lung cancer tissues (R = −0.596, P = 0.002). Compared with A549-miR-NC cells, the expression of COX-2 was significantly decreased in A549 cells transfected with miR-101 (P < 0.001). The proliferation of A549 cells was markedly inhibited after transfection of miR-101. The in vivo tumor growth of A549 cells transfected with miR-101 was significantly slower than wide type A549 cells.ConclusionMiR-101 expression is decreased in lung cancer, inducing an increase in COX-2 level. Enforced expression of miR-101 can remarkably reduce the cell proliferation and invasion ability of lung cancer cells.

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Relationship between tumour angiogenesis and expression of cyclo-oxygenase-2 and vascular endothelial growth factor-A in human renal cell carcinoma

Cited by 7 publications

References 34 publications

Evidence for the involvement of COX-2/VEGF and PTEN/Pl3K/AKT pathway the mechanism of oroxin B treated liver cancer

Evidence for the involvement of COX-2/VEGF and PTEN/Pl3K/AKT pathway the mechanism of oroxin B treated liver cancer

Epoxymicheliolide, a novelguaiane-type sesquiterpene lactone, inhibits NF‑κB/COX‑2 signaling pathways by targeting leucine�281 and leucine�25 in IKKβ in renal cell carcinoma

Micro ribonucleic acid (RNA)‐101 inhibits cell proliferation and invasion of lung cancer by regulating cyclooxygenase‐2

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