Effect of endostar combined with cisplatin on expression of VEGF and Sema3A of Lewis lung cancer rats

Feng, Ping; Zhang, Zhilin; Zhang, Zhihua; Zhang, Xiulong; Xu, Feng; Tang, Jianhua; Xiang, Bao-Li

doi:10.1016/s1995-7645(12)60201-6

Cited by 5 publications

(4 citation statements)

References 11 publications

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“…A previous study reported that metformin decreased vascular permeability and expression of VEGF, suggesting that metformin normalizes vascular permeability by regulating VEGF levels (26). Additionally, the effects of metformin and DDP on VEGF modulation have been also described in ovarian cancer in vivo and in Lewis lung cancer rats (3,27). In the present study, metformin alone or in combination with DDP was demonstrated to significantly decrease levels of VEGF and VEGFR2 in HO-8910 cells in a concentration-dependent manner, implicating VEGF/VEGFR2 in the ERK1/2-dependent anticancer effects of metformin and DDP in ovarian cancer.…”

Section: Discussionmentioning

confidence: 93%

Metformin in combination with cisplatin inhibits cell viability and induces apoptosis of human ovarian cancer cells by inactivating ERK 1/2

et al. 2017

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Abstract. Metformin protects against insulin resistance by restoring insulin sensitivity and may also possess anticancer activity. The aim of the present study was to investigate the effects of metformin alone or combined with cisplatin (DDP) on the cell viability and apoptosis of HO-8910 human ovarian cancer cells, and to investigate metformin as a potential novel therapeutic for treating ovarian cancer.

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Section: Discussionmentioning

confidence: 93%

Metformin in combination with cisplatin inhibits cell viability and induces apoptosis of human ovarian cancer cells by inactivating ERK 1/2

et al. 2017

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“…A clinical study by Masato Shingyoji also revealed that abnormal growth of lung cells in patient is because of the over-expression of VEGF [159]. Various report on anti-VEGF therapy including endostar combined with cisplatin on the expression of VEGF lewis lung cancer rats [100]. Various synthetic drugs are in clinical phase for their possible use in the treatment of lung cancer targeting VEGF and FGF-2 and their toxicity study data are mentioned in Table 3.…”

Section: Lung Cancermentioning

confidence: 99%

VEGF and FGF-2: Promising targets for the treatment of respiratory disorders

Laddha

Kulkarni

2019

Respiratory Medicine

124

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The endothelial cells play a crucial role in the progression of angiogenesis, which causes cell re-modulation, proliferation, adhesion, migration, invasion and survival. Angiogenic factors like cytokines, cell adhesion molecules, growth factors, vasoactive peptides, proteolytic enzymes (metalloproteinases) and plasminogen activators bind to their receptors on endothelial cells and activate the signal transduction pathways like epidermal growth factor receptor (EGFR phosphatidylinositol 3-kinase and (PI3K)/AKT/mammalian target of rapamycin (mTOR) which initiate the process of angiogenesis.Cytokines that stimulate angiogenesis include direct and indirect proangiogenic markers. The direct proangiogenic group of markers consists of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2) and hepatocyte growth factor (HGF) whereas the indirect proangiogenic markers include transforming growth factor-beta (TGF-β), interleukin 6 (IL-6), interleukin 8 (IL-8) and platelet-derived growth factor (PDGF).VEGF and FGF-2 are the strongest activators of angiogenesis which stimulate migration and proliferation of endothelial cells in existing vessels to generate and stabilize new blood vessels. VEGF is released in hypoxic conditions as an effect of the hypoxia-inducible factor (HIF-1α) and causes re-modulation and inflammation of bronchi cell. Cell re-modulation and inflammation leads to the development of various lung disorders like pulmonary hypertension, chronic obstructive pulmonary disease, asthma, fibrosis and lung cancer.This indicates that there is a firm link between overexpression of VEGF and FGF-2 with lung disorders. Various natural and synthetic drugs are available for reducing the overexpression of VEGF and FGF-2 which can be helpful in treating lung disorders. Researchers are still searching for new angiogenic inhibitors which can be helpful in the treatment of lung disorders.The present review emphasizes on molecular mechanisms and new drug discovery focused on VEGF and FGF-2 inhibitors and their role as anti-angiogenetic agents in lung disorders.

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“…Various studies investigated the effects of anti-VEGF medication, particularly end star in combination with cisplatin, Lewis lung cancer rat's VEGF expression. [39]…”

Section: Lung Cancermentioning

confidence: 99%

Untitled

2023

IJPBA

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Respiratory disorder is one of the common disorders related to the respiratory tract. In regards, to the development of resistance against the drugs now in use, respiratory disorders become a significant major challenge in the health sector. For respiratory illness treatment, many phytoleads or phytoconstituents are traditionally used and for their efficacy, few have been found with optimistic results. In this review, all the phytoleads or phytoconstituents have anti-inflammatory activity, and some of them possess antioxidant activity too. All are used to treat respiratory tract inflammation. Curcumin was used as an anti-asthmatic also. The results of this study show that for the cure of respiratory system disorders, phytoleads or phytoconstituents are used.The use of Phytoleads nowadays provide benefit in the discovery of new drugs for future targets.

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Effect of endostar combined with cisplatin on expression of VEGF and Sema3A of Lewis lung cancer rats

Abstract: ED combined with DDP could control the tumor growth effectively, and avoid weight loss. ED could reduce VEGF expression, and enhance Sema3A expression. Tumor vessel presents transient normalization. It is easy for DDP perfusion, and to kill tumor cells.

Cited by 5 publications

References 11 publications

Metformin in combination with cisplatin inhibits cell viability and induces apoptosis of human ovarian cancer cells by inactivating ERK 1/2

Metformin in combination with cisplatin inhibits cell viability and induces apoptosis of human ovarian cancer cells by inactivating ERK 1/2

VEGF and FGF-2: Promising targets for the treatment of respiratory disorders

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