Nerve growth factor and its high-affinity receptor trkA participate in the control of vascular endothelial growth factor expression in epithelial ovarian cancer

Campos, Ximena; Muñoz, Yenny; Selman, Alberto; Yazigi, R; Moyano, Leonor; Weinstein‐Oppenheimer, Caroline; Lara, Hernán E.; Romero, Carmen

doi:10.1016/j.ygyno.2006.07.007

Cited by 67 publications

(77 citation statements)

References 34 publications

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“…In addition, a correlative analysis suggests a function for NGF in ovarian cancer angiogenesis (Davidson et al, 2003). It is not yet known if NGF can exert a direct and/ or indirect action, as NGF can also induce the expression of pro-angiogenic factors such as VEGF (Campos et al, 2007). Clearly, it needs to be clarified how TrkA overexpressing tumor cells can stimulate tumor angiogenesis, but our present findings show that TrkA impact in breast carcinogenesis may also encompass angiogenesis.…”

Section: Discussionmentioning

confidence: 66%

TrkA overexpression enhances growth and metastasis of breast cancer cells

et al. 2009

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The Trk family of neurotrophin tyrosine kinase receptors is emerging as an important player in carcinogenic progression in non-neuronal tissues. Here, we show that breast tumors present high levels of TrkA and phospho-TrkA compared to normal breast tissues. To further evaluate the precise functions of TrkA overexpression in breast cancer development, we have performed a series of biological tests using breast cancer cells that stably overexpress TrkA. We show that (1) TrkA overexpression promoted cell growth, migration and invasion in vitro; (2) overexpression of TrkA per se conferred constitutive activation of its tyrosine kinase activity; (3) signal pathways including PI3K-Akt and ERK/ p38 MAP kinases were activated by TrkA overexpression and were required for the maintenance of a more aggressive cellular phenotype; and (4) TrkA overexpression enhanced tumor growth, angiogenesis and metastasis of xenografted breast cancer cells in immunodeficient mice. Moreover, recovered metastatic cells from the lungs exhibited enhanced anoikis resistance that was abolished by the pharmacological inhibitor K252a, suggesting that TrkA-promoted breast tumor metastasis could be mediated at least in part by enhancing anoikis resistance. Together, these results provide the first direct evidence that TrkA overexpression enhances the tumorigenic properties of breast cancer cells and point to TrkA as a potential target in breast cancer therapy.

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Section: Discussionmentioning

confidence: 66%

TrkA overexpression enhances growth and metastasis of breast cancer cells

et al. 2009

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“…It is therefore possible that BDNF/NTRK2-mediated signalling, coupled with crosstalk from other pathways, may be associated with tumour metastasis and chemotherapeutic resistance in ovarian cancer, making NTRK2 a putative therapeutic target (reviewed in Siu et al (2009)). It has been shown that NGF and NTRK1 are expressed at very low levels in normal ovarian surface epithelium but are significantly more abundant in epithelial ovarian cancer cells (Campos et al 2007, Tapia et al 2011. Furthermore, NGF has been shown to dose dependently up-regulate vascular endothelial growth factor (VEGF) isoform expression in cancer explants (Campos et al 2007), also increasing the proliferation, migration and differentiation of cultured ovarian cancer cells (Tapia et al 2011), effects that were inhibited by either a NGF antibody or a K252a.…”

Section: Potential Clinical Significancementioning

confidence: 99%

“…It has been shown that NGF and NTRK1 are expressed at very low levels in normal ovarian surface epithelium but are significantly more abundant in epithelial ovarian cancer cells (Campos et al 2007, Tapia et al 2011. Furthermore, NGF has been shown to dose dependently up-regulate vascular endothelial growth factor (VEGF) isoform expression in cancer explants (Campos et al 2007), also increasing the proliferation, migration and differentiation of cultured ovarian cancer cells (Tapia et al 2011), effects that were inhibited by either a NGF antibody or a K252a. These findings were corroborated by Julio-Pieper et al …”

Section: Potential Clinical Significancementioning

confidence: 99%

The roles of glial cell line-derived neurotrophic factor, brain-derived neurotrophic factor and nerve growth factor during the final stage of folliculogenesis: a focus on oocyte maturation

Linher‐Melville¹,

Li²

2013

Reproduction

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Neurotrophic factors were first identified to promote the growth, survival or differentiation of neurons and have also been associated with the early stages of ovarian folliculogenesis. More recently, their effects on the final stage of follicular development, including oocyte maturation and early embryonic development, have been reported. Glial cell line-derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), which are expressed in numerous peripheral tissues outside of the CNS, most notably the ovary, are now known to stimulate oocyte maturation in various species, also enhancing developmental competence. The mechanisms that underlie their actions in antral follicles, as well as the targets ultimately controlled by these factors, are beginning to emerge. GDNF, BDNF and NGF, alone or in combination, could be added to the media currently utilized for in vitro oocyte maturation, thereby potentially increasing the production and/or quality of early embryos.Reproduction (2013) 145 R43-R54

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“…El proceso de angiogénesis se refleja en la alta expresión de VEGF (estimulada en parte por NGF), y de su transcrito en COE respecto a ovarios normales [24][25][26] . Lo anterior contribuiría al alto crecimiento, y agresividad (metástasis) del cáncer de ovario lo que se traduce en una baja tasa de sobrevida 27 .…”

Section: Cáncer De Ovariounclassified

“…Estas últimas constituyen las principales moléculas secretadas por el tejido adiposo y son principalmente la leptina y adiponectina [33][34][35] . Además, los adipocitos secretan VEGF y estróge-nos, los cuales contribuyen al desarrollo de la angiogénesis y proliferación celular respectivamente en el cáncer de ovario 26,36 .…”

Section: Tejido Adiposo Y Su Asociación Con Cáncer De Ovariounclassified

Asociación entre obesidad y cáncer de ovario

2014

Self Cite

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L a obesidad es una enfermedad multifactorial producida por la interacción de factores genéticos y ambientales causados por el estilo de vida. Se caracteriza por un aumento excesivo de la grasa corporal, producido por un desequilibrio en el control homeostático mantenido en el tiempo, entre la energía consumida en la dieta y el gasto energético total 1-4 .En países desarrollados y en vías de desarrollo existe un aumento en la prevalencia de obesidad, tanto en la población infantil como adulta 5,6 . En Chile, también se observa un aumento de la obesidad, donde 25,1% de los adultos presenta obesidad (definido como índice de masa corporal IMC ≥ 30) (encuesta nacional de salud MINSAL 2010. www.minsal.cl).Debido a la condición fisiológica que se produce en la obesidad, esta constituye un factor de riesgo para diferentes patologías, entre las cuales se encuentran la diabetes tipo 2, hipertensión arterial, patologías cardiovasculares, y diferentes tipos de cáncer 2,3,7 . En este sentido, la obesidad ha sido fuertemente asociada con cánceres de origen ginecológico como el de mama y endometrio [8][9][10] , sin embargo, con el cáncer de ovario la asociación encontrada es menos clara, y existen diferentes estudios al respecto.En un meta-análisis de mujeres pre menopáusicas se estableció un aumento de 16% en desarrollar cáncer de ovario en mujeres adultas con sobrepeso (IMC entre 25 y 29 Kg/m 2 ) y el riesgo aumenta a 30% en mujeres obesas (IMC ≥ 30 Kg/m 2 ) 11 . Por otro lado, un estudio prospectivo de cohorte establece que un IMC ≥ 30 Kg/ m 2 tiene un riesgo relativo de 1,3 de desarrollar cáncer de ovario en mujeres pre-menopáusicas; sin embargo, dicha asociación no se observa en mujeres post-menopáusicas 12 . En concordancia con esto, un estudio poblacional muestra que las mujeres obesas que no utilizan terapia de reemplazo hormonal tienen un riesgo mayor (80%) de desarrollar cáncer de ovario respecto a las mujeres de peso normal 13 . Finalmente, lo anterior se relaciona con un meta-análisis reciente donde se encuentra que las personas no obesas tendrían una mejor sobrevida al cáncer de ovario versus las obesas y que esta asociación podría relacionarse con las características histológicas del cáncer 14,15 .La presente revisión tiene como objetivo presentar los antecedentes que específicamente

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Nerve growth factor and its high-affinity receptor trkA participate in the control of vascular endothelial growth factor expression in epithelial ovarian cancer

Cited by 67 publications

References 34 publications

TrkA overexpression enhances growth and metastasis of breast cancer cells

TrkA overexpression enhances growth and metastasis of breast cancer cells

The roles of glial cell line-derived neurotrophic factor, brain-derived neurotrophic factor and nerve growth factor during the final stage of folliculogenesis: a focus on oocyte maturation

Asociación entre obesidad y cáncer de ovario

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