Unidirectional crosstalk between Bcl-xL and Bcl-2 enhances the angiogenic phenotype of endothelial cells

Karl, Elisabeta; Zhang, Z; Dong, Zhihong; Neiva, Kathleen G.; Soengas, Marı́a S.; Koch, Alisa E.; Polverini, Peter J.; Núñez, Gabriel; Nör, Jacques E.

doi:10.1038/sj.cdd.4402174

Cited by 41 publications

(36 citation statements)

References 32 publications

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“…Incubation of human dermal microvascular EC with VEGF results in upregulation of bcl-2 in a VEGF receptor dependent manner. This promotes capillary morphogenesis of EC through activation of nuclear factor-B (NF-B) and production of CXC chemokines (19,20). It is presently not clear whether similar pathways are functional in vivo and/or in retinal EC.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of retinal endothelial cell migration and capillary morphogenesis in the absence of bcl-2

Kondo

Tang²,

Scheef³

et al. 2008

American Journal of Physiology-Cell Physiology

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Section: Discussionmentioning

confidence: 99%

Attenuation of retinal endothelial cell migration and capillary morphogenesis in the absence of bcl-2

Kondo

Tang²,

Scheef³

et al. 2008

American Journal of Physiology-Cell Physiology

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“…BCL-2 family proteins, might counteract antiproliferative or proapoptotic effects of celecoxib on the tumour endothelium or the lung cancer cells directly. 15 Interestingly, preclinical findings indicate that VEGF may in fact rescue cancer cells from celecoxib-induced apoptosis 16 and that anti-metastatic effects of coxibs may improve during simultaneous VEGF blockade. 17 A reasonable hypothesis, therefore, is that VEGF might counteract antitumour effects of celecoxib and related drugs.…”

Section: Discussionmentioning

confidence: 99%

Predictive role of plasma vascular endothelial growth factor for the effect of celecoxib in advanced non-small cell lung cancer treated with chemotherapy

Sörenson¹,

Fohlin²,

Lindgren³

et al. 2013

European Journal of Cancer

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Aim of the study: The primary purpose of this study is to investigate if pretreatment plasma levels of vascular endothelial growth factor (VEGF) are predictive of the effect of celecoxib on survival in advanced non-small cell lung cancer (NSCLC) treated with palliative chemotherapy. A secondary objective is to describe the course of plasma VEGF levels during and after treatment with cytotoxic chemotherapy combined with celecoxib or placebo. Methods: In a previously published double-blind multicenter phase III trial, 316 patients with NSCLC stage IIIB or IV and World Health Organisation (WHO) performance status 0-2 were randomised to receive celecoxib 400 mg b.i.d. or placebo in combination with two-drug platinum-based chemotherapy. Chemotherapy cycle length was three weeks and planned duration of chemotherapy was four cycles. Celecoxib was given for a maximum of one year but was stopped earlier in case of disease progression or prohibitive toxicity. In a subset of patients, plasma VEGF levels were examined at onset of treatment and at 6, 12 and 20 weeks. Results: VEGF levels at start of treatment were obtained in 107 patients at four study sites. The median value was 70 pg/ml. Mean values declined during the first 12 weeks and then increased at 20 weeks. A subpopulation treatment effect pattern plot (STEPP) analysis showed an inverse relationship between initial plasma VEGF and the impact of celecoxib on survival with zero effect at 200 pg/ml. The effect on survival by celecoxib in the whole subset of patients was positive (hazard ratio (HR) = 0.64 [confidence interval (CI) 0.43-0.95], p = 0.028). Conclusion: Low pretreatment plasma levels of VEGF appear to be predictive of a positive effect of celecoxib on survival.European Journal of Cancer (2012) xxx, xxx-xxx A v a i l a b l e a t w w w . s c i e n c e d i r e c t . c

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“…As with Bcl-2 in melanoma, Bcl-X L was found to be involved in the regulation of blood vessel formation through stimulating the expression of pro-angiogenic CXCL8 [53]. Including the fact that Bcl-X L can also stimulate Bcl-2 expression via VEGF and therefore creates a functional crosstalk demonstrating angiogenesis-promoting effects [54], targeting both of these proteins can provide a desirable therapeutic approach for melanoma patients. Accordingly, silencing of both Bcl-X L and Bcl-2 by the bispecific antisense oligonucleotide 4625 led to cell death in melanomas of all-stages [51].…”

Section: Bcl-x Lmentioning

confidence: 97%

Anti-apoptotic proteins on guard of melanoma cell survival

Hartman

Czyż

2013

Cancer Letters

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Unidirectional crosstalk between Bcl-xL and Bcl-2 enhances the angiogenic phenotype of endothelial cells

Cited by 41 publications

References 32 publications

Attenuation of retinal endothelial cell migration and capillary morphogenesis in the absence of bcl-2

Attenuation of retinal endothelial cell migration and capillary morphogenesis in the absence of bcl-2

Predictive role of plasma vascular endothelial growth factor for the effect of celecoxib in advanced non-small cell lung cancer treated with chemotherapy

Anti-apoptotic proteins on guard of melanoma cell survival

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