Celecoxib Can Induce Vascular Endothelial Growth Factor Expression and Tumor Angiogenesis

Xu, Kaiming; Gao, Huiying; Shu, Hui‐Kuo G.

doi:10.1158/1535-7163.mct-10-0415

Cited by 35 publications

(38 citation statements)

References 43 publications

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“…For example, PTEN phosphorylation appears to be upregulated in leukemia cancer cells compared to normal thymocytes through decreased CK2 expression and activity [32]. Increased PTEN phosphorylation at Ser-380 has also been observed in gastric tumors, and Notch signaling appears to regulate PTEN phosphorylation in pancreatic cancer cells [63, 64]. This provides a mechanism of PTEN inactivation in cancers where no loss of PTEN expression is observed.…”

Section: Pten Regulation By Post-translational Modificationsmentioning

confidence: 99%

PTEN function: the long and the short of it

Hopkins

Hodakoski

Barrows

et al. 2014

Trends in Biochemical Sciences

252

208

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Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a phosphatase that is frequently altered in cancer. PTEN has phosphatase-dependent and - independent roles; and genetic alterations in PTEN lead to deregulation of protein synthesis, cell cycle, migration, growth, DNA repair, and survival signaling. PTEN localization, stability, conformation, and phosphatase activity are controlled by an array of protein-protein interactions and post-translational modifications. Thus, PTEN-interacting and modifying proteins have profound effects on PTEN’s tumor suppressive functions. Moreover, recent studies identified mechanisms by which PTEN can exit cells, either via exosomal export or secretion, and act on neighboring cells. This review focuses on modes of PTEN protein regulation and ways in which perturbations in this regulation may lead to disease.

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Section: Pten Regulation By Post-translational Modificationsmentioning

confidence: 99%

PTEN function: the long and the short of it

Hopkins

Hodakoski

Barrows

et al. 2014

Trends in Biochemical Sciences

252

208

View full text Add to dashboard Cite

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“…In this context Wei et al reported in 2004 that celecoxib inhibits VEGF expression and reduces angiogenesis and metastasis of human pancreatic cancer via suppression of Sp1 transcription factor activity (Wei et al, 2004). Additionally, and in contrast to its previously mentioned anti-angiogenic profile, researchers have shown that celecoxib can induce VEGF expression and tumor angiogenesis (Xu et al, 2011). …”

Section: Pyrazoles Synthesismentioning

confidence: 93%

Pyrazoles as potential anti-angiogenesis agents: a contemporary overview

Kasiotis¹,

Tzanetou²,

Haroutounian³

2014

Front. Chem.

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Angiogenesis is a mulit-step process by which new blood vessels are formed from preexisting vasculature. It is a key rate limiting factor in tumor growth since new blood vessels are necessary to increase tumor size. In this context it has been shown that anti-angiogenic factors can be used in cancer therapy. Among the plethora of heterocyclic compounds administered as anti-angiogenesis agents, pyrazoles constitute one of the bottlenecks of this category. Currently, several pyrazole based compounds are administered or are in Phase II and III trials and new targets emerge. It is highly possible that the advent of the next two decades will lead to the discovery and use of additional pyrazoles whose anti-angiogenic profile will position them in the forefront of the battle of various malignancies. The present review is an attempt to focus on those pyrazoles that arise as anti-angiogenesis agents commenting both on the chemistry and bioactivity that these exhibit aiming to contribute to the perspectives that they hold for future research.

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“…Flank tumor frozen sections (5 μm) were fixed in cold methanol and stained with rat anti-mouse CD31 monoclonal antibody (BD Biosciences) as previously described [47]. CD31-stained slides were observed by fluorescent microscopy and images captured by an associated digital camera.…”

Section: Methodsmentioning

confidence: 99%

COX-2 overexpression increases malignant potential of human glioma cells through Id1

Wang

Shu

2013

Oncotarget

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Increased COX-2 expression directly correlates with glioma grade and is associated with shorter survival in glioblastoma (GBM) patients. COX-2 is also regulated by epidermal growth factor receptor signaling which is important in the pathogenesis of GBMs. However, COX-2 expression has not been previously shown to directly alter malignancy of GBMs. Id1 is a member of the helix-loop-helix (HLH) family of transcriptional repressors that act as dominant-negative inhibitors of basic-HLH factors. This factor has been shown to be regulated by COX-2 in breast carcinoma cells and recent studies suggest that Id1 may also be involved in the genesis/progression of gliomas. We now show that COX-2 increases the aggressiveness of GBM cells. GBM cells with COX-2 overexpression show increased growth of colonies in soft agar. Tumorigenesis in vivo is also increased in both subcutaneous flank and orthotopic intracranial tumor models. COX-2 overexpression induces Id1 expression in two GBM cell lines suggesting a role for Id1 in glioma transformation/tumorigenesis. Furthermore, we find direct evidence of a role for Id1 with significant suppression of in vitro transformation and in vivo tumorigenesis in COX-2-overexpressing GBM cells where Id1 has been knocked down. In fact, Id1 is even more efficient at enhancing transformation/tumorigenesis of GBM cells than COX-2. Finally, GBM cells with COX-2 or Id1 overexpression show greater migration/invasive potential and tumors that arise from these cells also display increased microvessel density, results in line with the increased malignant potential seen in these cells. Thus, COX-2 enhances the malignancy of GBM cells through induction of Id1.

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Celecoxib Can Induce Vascular Endothelial Growth Factor Expression and Tumor Angiogenesis

Abstract: Increased COX-2

Cited by 35 publications

References 43 publications

PTEN function: the long and the short of it

PTEN function: the long and the short of it

Pyrazoles as potential anti-angiogenesis agents: a contemporary overview

COX-2 overexpression increases malignant potential of human glioma cells through Id1

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