====== Meningioma cell line ======

Findings demonstrate the relevance of [[meningioma]] [[cell line]]s as a model system, especially as tools to investigate the [[signaling pathway]]s of, and subsequent resistance to, therapeutics currently in [[clinical trial]]s
((Mei Y, Bi WL, Greenwald NF, Agar NY, Beroukhim R, Dunn GP, Dunn IF. Genomic profile of human meningioma cell lines. PLoS One. 2017 May 26;12(5):e0178322. doi: 10.1371/journal.pone.0178322. PMID: 28552950; PMCID: PMC5446134.))
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[[CH-157MN]]

[[Ben-Men-1]]

[[IOMM-Lee]]
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Püttmann et al. developed a meningioma [[cell line]] by retroviral [[transduction]] of primary cells derived from a human [[World Health Organization grade 1 meningioma]] ([[meningothelial meningioma]]) with the [[human telomerase reverse transcriptase]] (h[[TERT]]) gene, which enables bypassing cellular senescence. Five [[clone]]s have been cultured for more than 21 months so far, while corresponding nontransfected cells ceased proliferation within 3 months. Quantitative RT-PCR and a [[telomeric repeat amplification protocol]] ([[TRAP]]) assay revealed high hTERT [[mRNA]] levels and high telomerase activity in all transduced populations, while nontransduced cells were negative. The average telomere size of transduced cells was considerably longer than that of parental cells and the [[biopsy]] specimen. One clone, designated [[Ben-Men-1]], was characterized in more detail, and exhibited typical cytological, immunocytochemical, ultrastructural and genetical features of meningioma, including whorl formation, expression of epithelial membrane antigen, desmosomes and interdigitating cell processes, as well as -22q. Following subdural transplantation into nude mice, tumor tissue with typical histological features of meningothelial meningioma was found. They conclude that Ben-Men-1 represents an immortalized yet differentiated cell line useful for biological and therapeutical studies on meningioma
((Püttmann S, Senner V, Braune S, Hillmann B, Exeler R, Rickert CH, Paulus W. Establishment of a benign meningioma cell line by hTERT-mediated immortalization. Lab Invest. 2005 Sep;85(9):1163-71. doi: 10.1038/labinvest.3700307. PMID: 15965488.)).
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Meningioma cell lines transplanted into flanks of nude mice exhibit microscopic, immunohistochemical, and ultrastructural features of meningiomas. The ease of monitoring tumor growth in the subcutaneous mouse flank model is its primary advantage, although an intracranial location is more biologically desirable
((Ragel BT, Couldwell WT, Gillespie DL, Wendland MM, Whang K, Jensen RL. A comparison of the cell lines used in meningioma research. Surg Neurol. 2008 Sep;70(3):295-307; discussion 307. doi: 10.1016/j.surneu.2007.06.031. Epub 2008 Feb 8. PMID: 18261772.)).
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Like most [[tumor]]s, [[meningioma]]s prefer anaerobic [[glycolysis]] for energy production ([[Warburg effect]]). This leads to an increased synthesis of the metabolite [[methylglyoxal]] (MGO). This [[metabolite]] is known to react with amino groups of [[protein]]s. This reaction is called [[glycation]], thereby building advanced glycation endproducts (AGEs). In a study, Selke et al investigated the influence of glycation on two [[meningioma cell line]]s, representing the WHO grade I ([[BEN-MEN-1]]) and the WHO grade III ([[IOMM-Lee]]). Increasing MGO concentrations led to the formation of AGEs and decreased growth in both cell lines. When analyzing the influence of [[glycation]] on [[adhesion]], [[chemotaxis]] and [[invasion]], they could show that the [[glycation]] of [[meningioma]] cells resulted in increased invasive potential of the benign meningioma [[cell line]], whereas the invasive potential of the malignant cell line was reduced. In addition, [[glycation]] increased the [[E-cadherin]]- and decreased the [[N-cadherin]]-expression in [[BEN-MEN-1]] cells, but did not affect the [[cadherin]]-expression in [[IOMM-Lee]] cells
((Selke P, Rosenstock P, Bork K, Strauss C, Horstkorte R, Scheer M. Glycation of benign meningioma cells leads to increased invasion. Biol Chem. 2021 Mar 17. doi: 10.1515/hsz-2020-0376. Epub ahead of print. PMID: 33725749.)).