VEGF elicits epithelial-mesenchymal transition (EMT) in prostate intraepithelial neoplasia (PIN)-like cells via an autocrine loop

Gonzalez-Moreno, Oscar; Lecanda, Jon; Green, Jeffrey E.; Segura, Víctor; Catena, Raúl; Serrano, Diego; Calvo, Alfonso

doi:10.1016/j.yexcr.2009.11.020

Cited by 103 publications

(81 citation statements)

References 34 publications

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“…Similarly, vimentin and TWIST1 expression have a positive feedback effect on HIF‐1 α through the activation of growth receptors related to the PI3K/mTOR/AKT signaling pathways 34, 35. Studies of xenografts in preinvasive cells demonstrated that the addition of VEGF induces the appearance of EMT markers 36, 37. Our study showed that the increase in VEGF expression is proportional to that of EMT markers in vivo, thereby, shortening OS.…”

Section: Discussionmentioning

confidence: 52%

Epithelial–mesenchymal transition, proliferation, and angiogenesis in locally advanced cervical cancer treated with chemoradiotherapy

Rojas‐Puentes

Cardona²,

Carranza³

et al. 2016

Cancer Medicine

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We evaluated the association between epithelial–mesenchymal transition (EMT)‐derived markers and expression of proteins associated with cell proliferation and tumor growth, as well as their prognostic roles, in 61 patients (mean age 52 ± 10 years) with locally advanced cervical cancer, all of whom were treated with chemoradiation and intracavitary brachytherapy. We used immunohistochemical analysis to assess the expression of proteins targeted in our investigation. Various statistical analyses were then conducted to assess protein marker associations with survival outcomes. Forty‐six percent of the patients were positive for human papilloma virus. Median progression‐free survival (PFS) was 6.6 months (95% confidence interval [CI]: 4.0–9.1, whereas overall survival (OS) was 30.0 months (95% CI: 11–48). Multivariate analysis demonstrated that vascular endothelial growth factor (VEGF) (P = 0.002), epidermal growth factor receptor (EGFR) (P = 0.001), and TWIST2 (P = 0.001) expression levels, as well as a tumor size <6 cm (P = 0.02), influenced OS. Changes in TWIST2 levels and loss of E‐cadherin expression were correlated with VEGF and EGFR levels; furthermore, patients with high TWIST2 expression had shorter OS (P = 0.0001), as those with loss of E‐cadherin (P = 0.02). OS was even shorter when positive EGFR or VEGF expression was related with EMT markers (positive EGFR + negative E‐cadherin: median 14 months, 95% CI: 3–24; negative EGFR + positive E‐cadherin: median 31 months, 95% CI: 14–NA; P = 0.02.). The presence of EMT markers was associated with proliferative and pro‐angiogenic protein expression and influenced the prognosis of locally advanced cervical cancer.

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Section: Discussionmentioning

confidence: 52%

Epithelial–mesenchymal transition, proliferation, and angiogenesis in locally advanced cervical cancer treated with chemoradiotherapy

Rojas‐Puentes

Cardona²,

Carranza³

et al. 2016

Cancer Medicine

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“…A previous study demonstrated that and VEGF (48) cytokines are secreted by neoplastic cells undergoing EMT. Furthermore, it has been reported that these two cytokines can co-operate to induce EMT (2) in prostate intraepithelial neoplasia-like cells via an autocrine loop (48).…”

Section: Vegfmentioning

confidence: 99%

“…Furthermore, it has been reported that these two cytokines can co-operate to induce EMT (2) in prostate intraepithelial neoplasia-like cells via an autocrine loop (48). MCF7 breast cancer cells are also able to undergo EMT via TWIST overexpression, and this was associated with increased synthesis of the angiogenic factor VEGF (49).…”

Section: Vegfmentioning

confidence: 99%

Epithelial-mesenchymal transition in cancer: Role of the IL-8/IL-8R axis

et al. 2017

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Abstract. Epithelial-mesenchymal transition (EMT) is a biological process that is associated with cancer metastasis and invasion. In cancer, EMT promotes cell motility, invasion and distant metastasis. Interleukin (IL)-8 is highly expressed in tumors and may induce EMT. The IL-8/IL-8R axis has a vital role in EMT in carcinoma, which is regulated by several signaling pathways, including the transforming growth factor β-spleen associated tyrosine kinase/Src-AKT/extracellular signal-regulated kinase, p38/Jun N-terminal kinase-activating transcription factor-2, phosphoinositide 3-kinase/AKT, nuclear factor-κB and Wnt signaling pathways. Blocking the IL-8/IL-8R signaling pathway may be a novel strategy to reduce metastasis and improve patient survival rates. This review will cover IL-8-IL-8R signaling pathway in tumor epithelial-mesenchymal transition.

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“…Uno de los potenciales factores pronósticos que se está estudiando ampliamente es el factor de crecimiento vascular endotelial (VEGF), por su relación, no sólo con la angiogénesis tumoral, sino también con otros fenómenos descritos más recientemente, como la transición epitelio-mesenquimática (EMT), inhibición de la apoptosis, capacidad migratoria de las células, capacidad adhesiva a la matriz y proliferación de las células tumorales por vías autocrinas y paracrinas [6][7][8][9][10][11][12][13] . El concepto de EMT en oncología es relativamente nuevo y podría reflejar un proceso de transdiferenciación en vez de un proceso de desdiferenciación 15 .…”

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Identificación de factor de crecimiento vascular endotelial en células glandulares de tejido prostético maligno y benigno: Relación con la recidiva tumoral al año de la prostatectomía

Acuña¹,

Ellwanger

Ramírez

et al. 2013

Rev. méd. Chile

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VEGF elicits epithelial-mesenchymal transition (EMT) in prostate intraepithelial neoplasia (PIN)-like cells via an autocrine loop

Cited by 103 publications

References 34 publications

Epithelial–mesenchymal transition, proliferation, and angiogenesis in locally advanced cervical cancer treated with chemoradiotherapy

Epithelial–mesenchymal transition, proliferation, and angiogenesis in locally advanced cervical cancer treated with chemoradiotherapy

Epithelial-mesenchymal transition in cancer: Role of the IL-8/IL-8R axis

Identificación de factor de crecimiento vascular endotelial en células glandulares de tejido prostético maligno y benigno: Relación con la recidiva tumoral al año de la prostatectomía

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