Growth Hormone Production and Action in N1E-115 Neuroblastoma Cells

Abstract

Neuroblastoma cells are undifferentiated cells derived from the neural crest and are commonly used as models for studying neural function. Mouse N1E-115 neuroblastoma cells are derived from cancerous tissue and provide a model for studying the oncogenesis of neural cells. As growth hormone (GH) has been implicated as an autocrine or paracrine involved in neural regulation and in the induction or progression of cancer, the possibility that N1E-115 cells are sites of GH production and GH action was assessed. Using RT-PCR, cultured N1E-115 cells were found to express the mouse GH and GH receptor (GHR) genes. Immunocytochemistry demonstrated that both of the translated proteins (GH and its receptor) were abundantly present in the cytoplasm of these cells and their co-localization was established by confocal cytochemistry. GH action in these cells was determined in cells cultured for 72 h in the presence or absence of 10(-6) M or 10(-9) M mouse GH, which induced neurite sprouting and increased axon growth. In summary, the expression of GH and its receptor in GH responsive tumor-derived N1E-115 neuroblastoma cells suggests they provide a useful experimental model to assess GH actions in neural function or neural oncogenesis.

Regenerative Effect of Growth Hormone (GH) in the Retina after Kainic Acid Excitotoxic Damage

“…It is important to note that the IPL is mostly formed by dendritic connections between bipolar cells, amacrine cells, and retinal ganglion cells (RGCs) [65], however, in the chicken, some displaced RGCs and glia could be observed within this layer [4]. Our findings are consistent with previous reports demonstrating neurotrophic effects of GH in neurite and axonal growth [6,7,66]. It is therefore possible that the GH-induced recovery in patients with brain trauma, cognitive deficit, and spinal cord injury, at least partially includes the restoration of functional neural interconnections [6,64,67,68].…”

Targeting growth hormone receptor in human melanoma cells attenuates tumor progression and epithelial mesenchymal transition via suppression of multiple oncogenic pathways

“…Unfortunately, several reports of resistance against even the latest chemotherapy, [7, 8] point to a pressing need for identifying novel targets in this cancer type which can help in diagnosis and therapy [2]. The highly proliferative effect of an induced autocrine-hGH system in endometrial and mammary carcinoma as well as upregulated migration, anchorage-free growth and propensity to epithelial mesenchymal transition is known [9, 10, 82–84]. The autocrine/paracrine action of human GH in oncogenic incidents has been further established in autocrine GH-driven miR-96-182-183 mediated upregulation of epithelial mesenchymal transition (EMT) in breast cancer [55, 63].…”

Growth Hormone (GH) and Gonadotropin-Releasing Hormone (GnRH) in the Central Nervous System: A Potential Neurological Combinatory Therapy?

“…However, in vitro, evidence shows that GH is able to induce IGF-I, and this growth factor is able to promote the proliferation and migration of brain cancer cells. In addition, GH is able to induce axonal growth in neuroblastoma cells [ 56 ]. Moreover, GH, GHR, and IGF-I have been detected within the same glioma cell, suggesting autocrine/paracrine actions that could be related to the resistance and aggressive behavior of this type of cancer [ 37 ].…”