497: Activation of TRKA receptor by nerve growth factor induces shedding of P75 receptor related with progression of epithelial ovarian cancer

Romero, Carmen; Vallejos, C.; Gabler, Fernando; Selman, Alberto; Vega, Margarita

doi:10.1016/s0959-8049(14)50442-x

Cited by 2 publications

(3 citation statements)

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“…ADAM17 is able to cause TRKA cleavage, facilitating cell survival and proliferation. Besides, upon TRKA activation through NGF binding, ADAM 17 cleaves p75 on its extracellular domain, and afterwards γ-secretase cleaves it on the intracellular domain [86]. The biological consequences of these processes are not completely understood.…”

Section: Neurotrophins and Their Role In Ovarian Cancermentioning

confidence: 99%

Role of Nerve Growth Factor (NGF) and miRNAs in Epithelial Ovarian Cancer

Retamales-Ortega

Oróstica

Vera

et al. 2017

IJMS

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Ovarian cancer is the eighth most common cancer in women worldwide, and epithelial ovarian cancer (EOC) represents 90% of cases. Nerve growth factor (NGF) and its high affinity receptor tyrosine kinase A receptor (TRKA) have been associated with the development of several types of cancer, including EOC; both NGF and TRKA levels are elevated in this pathology. EOC presents high angiogenesis and several molecules have been reported to induce this process. NGF increases angiogenesis through its TRKA receptor on endothelial cells, and by indirectly inducing vascular endothelial growth factor expression. Other molecules controlled by NGF include ciclooxigenase-2, disintegrin and metalloproteinase domain-containing protein 17 (ADAM17) and calreticulin (CRT), proteins involved in crucial processes needed for EOC progression. These molecules could be modified through microRNA regulation, which could be regulated by NGF. MicroRNAs are the widest family of non-coding RNAs; they bind to 3′-UTR of mRNAs to inhibit their translation, to deadenilate or to degraded them. In EOC, a deregulation in microRNA expression has been described, including alterations of miR-200 family, cluster-17-92, and miR-23b, among others. Since the NGF-microRNA relationship in pathologies has not been studied, this review proposes that some microRNAs could be associated with NGF/TRKA activation, modifying protein levels needed for EOC progression.

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Section: Neurotrophins and Their Role In Ovarian Cancermentioning

confidence: 99%

Role of Nerve Growth Factor (NGF) and miRNAs in Epithelial Ovarian Cancer

Retamales-Ortega

Oróstica

Vera

et al. 2017

IJMS

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show abstract

“…The NGF/TRKA signaling pathway has also been linked to several transduction cascades that stimulate cancer progression, including VEGF production and secretion [26], the COX2/PGE2 inflammatory response [28], ADAM17 activity [29] and alterations on calreticulin (CRT) subcellular localization [30]. All the molecules mentioned above have a role in the development or progression of ovarian cancer by altering processes such as inflammation, angiogenesis, immune evasion, survival and metastasis.…”

Section: Roles Of Nerve Growth Factor In the Normal Ovary And In Epitmentioning

confidence: 99%

“…The p75-ICD, on the other hand, increases TRKA activation, potentially inducing pro-carcinogenic processes. Besides, NGF stimulation activates TRKA, ADAM17 and γ-secretase, reducing p75 NTR levels and increasing p75-CTF and p75-ICD levels, favoring cell survival [29]. Also, there is evidence that suggests that p75-ICD could act as a transcription regulator, enhancing TRKA cancer activity [51].…”

Section: Roles Of Nerve Growth Factor In the Normal Ovary And In Epitmentioning

confidence: 99%

Signaling Pathways Related to Nerve Growth Factor and miRNAs in Epithelial Ovarian Cancer

Vera¹,

Retamales-Ortega²,

Garrido³

et al. 2018

Ovarian Cancer - From Pathogenesis to Treatment

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Epithelial ovarian cancer (EOC) is a disease that causes 140,000 deaths every year. Nerve growth factor (NGF) and its high affinity receptor TRKA play important roles in follicular maturation, follicle-stimulating hormone (FSH) receptor acquisition and ovulation in normal ovary. Also, NGF has many roles in EOC cells: increasing survival, proliferation, cyclooxigenase-2 (COX-2), vascular endothelial growth factor (VEGF) and metalloproteinase ADAM17 expression. Besides, NGF inhibits calreticulin translocation from the endoplasmic reticulum to cell surface, possibly diminishing the efficacy of immunogenic therapies in EOC. Additionally, NGF acts as an angiogenic factor by a direct stimulation of migration, differentiation and proliferation of endothelial cells. Among the numerous factors actually described to be important in many types of cancer, including EOC, are the microRNAs (miRs). Indeed, it has been found that miR-143 is downregulate in EOC, which correlates with an increase of COX-2; concomitantly, NGF increases COX-2 as mentioned. Furthermore, NGF increases miR-222 and its target is the metalloproteinase inhibitor TIMP3, increasing the ADAM17 function. Also, NGF increases cMYC transcription factor in EOC, which decreases miR-23 levels regulating proteins involved in cell cycle and tumor growth. Therefore, NGF/TRKA signaling pathways alter the expression of many proteins and deregulate miRs in EOC, leading to the progression of this cancer.

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497: Activation of TRKA receptor by nerve growth factor induces shedding of P75 receptor related with progression of epithelial ovarian cancer

Cited by 2 publications

References 0 publications

Role of Nerve Growth Factor (NGF) and miRNAs in Epithelial Ovarian Cancer

Role of Nerve Growth Factor (NGF) and miRNAs in Epithelial Ovarian Cancer

Signaling Pathways Related to Nerve Growth Factor and miRNAs in Epithelial Ovarian Cancer

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