PubMed · 7792694
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M Arteaga-Treviño, C J Abood. 1995. The different classification systems for astrocytomas.. https://doi.org/10.1016/0090-3019(95)80015-9
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Elastin has been identified within the meninges and the microvasculature of the normal human brain. However, the role that elastin plays in either facilitating astrocytoma cell attachment to these structures or modulating astrocytoma invasion has not been previously characterized. We have recently shown that astrocytoma cell lines and specimens produce tropoelastin, and express the 67 kDa elastin binding protein (EBP). In the present report, we have established that astrocytoma cells attach to elastin as a substrate in vitro. The U87 MG astrocytoma cell line demonstrated the greatest degree of adhesion. In addition, all astrocytoma cell lines examined were capable of penetrating and migrating through an intact elastin membrane, and of degrading tritiated-elastin, a process that could be prevented by the pre-incubation of astrocytoma cells with EDTA, but not with alpha1-antitrypsin. Astrocytoma cells were also capable of penetrating 1 mm sections of human brain tissue maintained as organotypic cultures. Interestingly, the invasive potential of cultured astrocytoma cells plated on organotypic cultures of human brain was significantly increased after exposure to elastin degradation products (kappa-elastin), which interact with astrocytoma cell surface EBP. Our data show that astrocytoma cells express a functional 67 kDa EBP, enabling them to potentially recognize and attach to elastin as a substrate. These data also suggest that this elastin receptor may be involved in processes which regulate regional astrocytoma invasion.
Mutation in the ras oncogene is one of the most commonly reported genetic aberrations in human cancer. Activated ras mutants are thought to play a major role in promoting the growth and malignancy of tumor cells. Ras protein plays a central role in transmitting mitogenic signals from cell surface-to-nucleus by activating signaling pathways in response to receptor activation. Ras protein by recruiting c-Raf-1 kinase to the plasma membrane activates the mitogen-activated protein (MAP) kinase pathway. Expression of activated ras mutants in rodent fibroblast has been reported to constitutively activate the MAP kinase pathway, suggesting that constitutive activation of this pathway contributes to Ras influence on proliferation and transformation. In this study, we investigated whether stable expression of an activated Ki-Ras oncogenic mutant (G12V) in human astrocytoma cells leads to constitutive activation of the MAP kinase pathway and how this may influence cellular proliferation and signaling by epidermal growth factor (EGF) receptor. We discovered that Ki-Ras stable expression does not lead to constitutive activation of the MAP kinase pathway, rather expression of Ki-Ras plays a role in attenuating the activation of this pathway in response to EGF stimulation. Furthermore, we provide evidence that stable Ki-Ras expression attenuates the ability of EGF receptor to activate the MAP kinase pathway by interfering with the receptor ability to autophosphorylate at tyrosine residues and not by down regulating receptor expression.
BACKGROUND: Opioid agonists can inhibit cell proliferation in various neural tumor cell lines, including rat gliomas. Because opioid antimitogenic effects are mediated by opioid receptors, it was of interest to the authors to determine opioid receptor levels in human brain tumors. METHODS: Specimens obtained at craniotomy from 30 patients with glioma and nonneoplastic brain disorders were evaluated for their kappa-opioid receptor binding. Kd and Bmax values were estimated from homologous competition binding curves with the kappa1-selective radioligand [3H]U69,593. RESULTS: Receptor binding density was greatest in nonneoplastic brain tissue, less in Grade 2 and 3 astrocytoma, and least in glioblastoma multiforme. CONCLUSIONS: These results suggest that opioid receptor-based stratification of grade may have clinical utility in distinguishing glioblastoma multiforme from lower grade astrocytomas, and thereby may facilitate diagnosis and treatment.