Expression of vascular endothelial growth factor (VEGF) and its cognate receptors in human pheochromocytomas

Takekoshi, Kazuhiro; Isobe, Kazumasa; Yashiro, Tohru; Hara, Hisato; Ishii, Kiyo‐aki; Kawakami, Yasushi; Nakai, Toshiaki; Okuda, Yukichi

doi:10.1016/j.lfs.2003.07.036

Cited by 30 publications

(28 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It can be secreted by colon carcinoma cells, via its interaction with its receptor VEGFR-2. It mediates many key components of angiogenesis, including endothelial cell proliferation, invasion, migration, and survival, as well as vessel permeability [21,22]. Inhibition of PGE 2 and VEGF expression can increase the apoptosis of colon cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Honokiol augments the anti-cancer effects of oxaliplatin in colon cancer cells

Hua¹,

Chen²,

Shen³

et al. 2013

ABBS

View full text Add to dashboard Cite

Oxaliplatin is an important drug in the chemotherapy of colorectal carcinoma, but its toxicity, especially dose-related neurosensory toxicity, is not well tolerated. In this study, we investigated whether honokiol could augment the anti-tumor effect of oxaliplatin in colon cancer HT-29 cells in vitro and whether honokiol could be used with oxaliplatin to decrease oxaliplatin dose. We used the normal colon cells, human colonic epithelial cells (HCoEpiCs) as control cells. Cell proliferation, apoptosis, prostaglandin E2 (PGE 2 ) and vascular endothelial growth factor (VEGF) levels were also investigated. Expression levels of cyclo-oxygenase 2 (COX-2), VEGF, AKT/p-AKT, extracellular signal-related kinase (ERK)1/2/p-ERK1/2, nuclear factor kappa B (NF-kB) P65/p-P65, and caspase-3 were measured. Honokiol or oxaliplatin suppressed the proliferation of HT-29 cells in a concentrationdependent manner, but only high concentrations of honokiol would suppress the proliferation of HCoEpiCs. HT-29 cells were more sensitive to oxaliplatin treatment in the presence of honokiol. Oxaliplatin combined with honokiol improved the apoptosis rate of HT-29 cell and reduced PGE 2 and VEGF secretion levels. Expression levels of COX-2 and VEGF protein and phosphorylation of AKT, ERK1/2, and NF-kB P65 were also inhibited. Caspase-3 levels were upregulated after honokiol treatment. Therefore, honokiol can be used in combination with oxaliplatin in the chemotherapy of colon cancer. This combination allows a reduction in oxaliplatin dose, and thereby reduces its adverse effects. It may also enhance the chemotherapeutic effect of oxaliplatin for this disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Honokiol augments the anti-cancer effects of oxaliplatin in colon cancer cells

Hua¹,

Chen²,

Shen³

et al. 2013

ABBS

View full text Add to dashboard Cite

show abstract

“…Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are emerging as the key regulators of tumor angiogenesis. VEGFs can stimulate angiogenesis and increase the permeability of capillaries after binding to VEGFRs [5][6][7]. VEGFR-2, also known as kinase insert domain receptor (KDR), is a key receptor involved in malignant angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of KDR expression induces apoptosis in breast cancer cells

Zhang

Yan

et al. 2014

Cellular and Molecular Biology Letters

View full text Add to dashboard Cite

Angiogenesis plays a crucial role in the growth, invasion and metastasis of breast cancer. Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are the key regulators of tumor angiogenesis. VEGFR-2, known as the kinase insert domain receptor (KDR), is a key receptor involved in malignant angiogenesis. We previously showed that knocking down KDR with short interference RNA (KDR-siRNA) markedly decreased KDR expression and suppressed tumor growth in a xenograft model. However, the mechanisms underlying the anti-cancer effects of KDR-siRNA are not clearly understood. This study aimed to elucidate the molecular mechanisms that induce apoptosis in human breast cancer MCF-7 cells after transfection with KDRsiRNA. We studied the effects of KDR-siRNA on proliferation, apoptosis, antiapoptotic and pro-apoptotic proteins, mitochondrial membrane permeability, cytochrome c release and caspase-3 activity. The results indicated that KDRsiRNA treatment significantly inhibited the proliferation and induced the apoptosis of MCF-7 cells, reduced the levels of the anti-apoptotic proteins, Bcl-2 and Bcl-xl, and increased the level of the pro-apoptotic protein Bax, resulting in a decreased Bcl-2/Bax ratio. KDR-siRNA also enhanced the mitochondrial membrane permeability, induced cytochrome c release from the mitochondria, upregulated apoptotic protease-activating factor-1 (Apaf-1), cleaved caspase-3, and increased caspase-3 activity in MCF-7 cells. Furthermore, KDR-siRNA-induced apoptosis in MCF-7 cells was blocked by the caspase inhibitor Z-VAD-FMK, suggesting a role of caspase activation in the induction of apoptosis. These results indicate that the Bcl-2 family proteins and caspase-related mitochondrial pathways are primarily involved in KDR-siRNAinduced apoptosis in MCF-7 cells and that KDR might be a potential therapeutic target for human breast cancer treatments.

show abstract

“…Anti-angiogenic molecules PCs are highly vascular, and aberrant angiogenesis has been associated with a malignant phenotype, especially in patients carrying SDHB gene mutations (Takekoshi et al 2004). PC tumours express higher levels of VEGF and its receptors (VEGF-R), suggesting they may play an important role in their pathogenesis (Takekoshi et al 2004).…”

Section: :6mentioning

confidence: 99%

“…PC tumours express higher levels of VEGF and its receptors (VEGF-R), suggesting they may play an important role in their pathogenesis (Takekoshi et al 2004). Interestingly, using antibodies against VEGF it was possible to reduce angiogenesis and tumour proliferation in a xenograft mouse model of PCs (Zielke et al 2002).…”

Section: :6mentioning

confidence: 99%

Molecular targeted therapies in adrenal, pituitary and parathyroid malignancies

Angelousi¹,

Dimitriadis²,

Zografos³

et al. 2017

Endocrine-Related Cancer

View full text Add to dashboard Cite

Tumourigenesis is a relatively common event in endocrine tissues. Currently, specific guidelines have been developed for common malignant endocrine tumours, which also incorporate advances in molecular targeted therapies (MTT), as in thyroid cancer and in gastrointestinal neuroendocrine malignancies. However, there is little information regarding the role and efficacy of MTT in the relatively rare malignant endocrine tumours mainly involving the adrenal medulla, adrenal cortex, pituitary, and parathyroid glands. Due to the rarity of these tumours and the lack of prospective studies, current guidelines are mostly based on retrospective data derived from surgical, locoregional and ablative therapies, and studies with systemic chemotherapy. In addition, in many of these malignancies the prognosis remains poor with individual patients responding differently to currently available treatments, necessitating the development of new personalised therapeutic strategies. Recently, major advances in the molecular understanding of endocrine tumours based on genomic, epigenomic, and transcriptome analysis have emerged, resulting in new insights into their pathogenesis and molecular pathology. This in turn has led to the use of novel MTTs in increasing numbers of patients. In this review, we aim to present currently existing and evolving data using MTT in the treatment of adrenal, pituitary and malignant parathyroid tumours, and explore the current utility and effectiveness of such therapies and their future evolution.

show abstract

Expression of vascular endothelial growth factor (VEGF) and its cognate receptors in human pheochromocytomas

Cited by 30 publications

References 32 publications

Honokiol augments the anti-cancer effects of oxaliplatin in colon cancer cells

Honokiol augments the anti-cancer effects of oxaliplatin in colon cancer cells

Downregulation of KDR expression induces apoptosis in breast cancer cells

Molecular targeted therapies in adrenal, pituitary and parathyroid malignancies

Contact Info

Product

Resources

About