Growth hormone and insulin-like growth factor-I: effects on the growth of glioma cell lines

Friend, Keith; Khandwala, Hasnain; Flyvbjerg, Allan; Hill, Hank C.; Li, J.; McCutcheon, Ian E.

doi:10.1054/ghir.2000.0183

Cited by 26 publications

(16 citation statements)

References 17 publications

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“…Similar findings have recently been reported on oestrogen receptor (ER)-positive mammary carcinoma cells [14]. On the other hand, another study that investigated the role of the GH/IGF-I axis on glioma cell lines demonstrated that, even in the presence of a low GH/IGF-I environment, the growth of glioma tumour cells could not be inhibited in vivo, suggesting the involvement of other signals for cell proliferation [15]. In agreement, intracellular signalling 'crosstalk' pathways have been identified between IGF-IR and the erbB family of receptors, which include erbB1 (EGFR) and erbB2 (HER2/neu), in ovarian and breast cancer, and IGF-IR and ER in breast cancer [4].…”

Section: Experimental Evidencesupporting

confidence: 81%

Growth hormone, insulin-like growth factor system and carcinogenesis

Boguszewski

Kopchick

2015

Endokrynologia Polska

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The growth hormone (GH) and insulin-like growth factor (IGF) system plays an important role in the regulation of cell proliferation, differentiation, apoptosis, and angiogenesis. In terms of cell cycle regulation, the GH-IGF system induces signalling pathways for cell growth that compete with other signalling systems that result in cell death; thus the final effect of these opposed forces is critical for normal and abnormal cell growth. The association of the GH-IGF system with carcinogenesis has long been hypothesised, mainly based on in vitro studies and the use of a variety of animal models of human cancer, and also on epidemiological and clinical evidence in humans. While ample experimental evidence supports a role of the GH-IGF system in tumour promotion and progression, with several of its components being currently tested as central targets for cancer therapy, the strength of evidence from patients with acromegaly, GH deficiency, or treated with GH is much weaker. In this review, we will attempt to consolidate this data. StreszczenieOś hormon wzrostu (GH)-insulinopodobny czynnik wzrostu (IGF) odgrywa istotną rolę w regulacji proliferacji i różnicowania komórek, apoptozy i angiogenezy. Oś GH-IGF wpływa na regulację cyklu komórkowego przez pobudzenie szlaku wzrostu komórki w stosunku do szlaków sygnałowych prowadzących do śmierci komórki, a ostateczny efekt oddziaływania tych dwóch sił ma podstawowe znaczenie dla prawidłowego lub nieprawidłowego wzrostu komórki. Hipotezy na temat powiązań osi GH-IGF z karcynogenezą pojawiły się wiele lat temu, głównie w oparciu o wyniki badań in vitro oraz badań z wykorzystaniem różnych zwierzęcych modeli raka występującego u ludzi. Chociaż liczne dane doświadczalne potwierdzają rolę osi GH-IGF sprzyjającą rozwojowi i progresji nowotworów, a nad kilkoma składowymi tej osi trwają obecnie badania oceniające ich przydatność jako główne cele terapii przeciwnowotworowej, to jednak siła dowodów uzyskanych u chorych z akromegalią, niedoborem GH lub osób leczonych GH jest znacznie słabsza. W niniejszej pracy przeglądowej spróbowano zebrać wszystkie te dane.

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Section: Experimental Evidencesupporting

confidence: 81%

Growth hormone, insulin-like growth factor system and carcinogenesis

Boguszewski

Kopchick

2015

Endokrynologia Polska

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“…2005;Favier et al 2007). The presence of GH and its receptor in these neural cells is thus of interest, since both have also been found in brain tumors and in glioma cell lines (Friend et al 2001), in which autocrine or paracrine actions of GH maybe responsible for the induction and/or progress of oncogenesis (Waters and Barclay 2007). Indeed, the oncogenic properties of GH in human tissues are exclusive to autocrine-produced GH (Perry et al 2006), as exogenously administered GH, mimicking the effects of pituitary GH, does not result in oncogenesis (Kaulsay et al 1999;Mukhina et al 2004;Zhu et al 2005).…”

Section: Discussionmentioning

confidence: 99%

“…The possibility that GH has a neurotrophic action in N1E-115 cells has therefore been assessed. Moreover, as autocrine or paracrine actions of GH have been implicated in the etiology and progression of cancer (Hull and Harvey 2006;Perry et al 2006;Waters and Barclay 2007), including glioma (Friend et al 2001), the possibility that N1E-115 cells, as model cancer cells, express the GH and GH receptor (GHR) genes has also been determined.…”

Section: Introductionmentioning

confidence: 99%

Growth Hormone Production and Action in N1E-115 Neuroblastoma Cells

et al. 2009

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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.

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“…The possibility that GH might be involved in the induction or progression of glioma is supported by the demonstration that a panel of immortalized glioma cell lines expressed the receptors of GH and IGF-1 and IGF-II (Friend et al, 2001). Malignant gliomas, moreover, express an increased number of IGF receptors in comparison with normal brain tissue (Merrill and Edwards, 1990) and exogenous IGF-1 increases glioma cell proliferation and migration (Schlenska-Lange et al, 2008).…”

Section: Gh and Gliomamentioning

confidence: 99%