Effect of ranolazine and eleclazine on glioblastomacell line
Başlık çevirisi mevcut değil.
- Tez No: 786908
- Danışmanlar: PROF. MUSTAFA BA DJAMGOZ
- Tez Türü: Yüksek Lisans
- Konular: Biyoloji, Biyomühendislik, Tıbbi Biyoloji, Biology, Bioengineering, Medical Biology
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2019
- Dil: İngilizce
- Üniversite: Rheinische Friedrich-Wilhelms-Universität Bonn
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 75
Özet
Özet yok.
Özet (Çeviri)
Glioblastoma is the most aggressive and highly invasive forms of brain tumour. Current treatments have not managed to significantly increase patients' survival and this resistance means that there is an urgent need for novel treatments. Hypoxia within the tumour mass and upregulation of voltage-gated sodium channels (VGSCs) are often involved in invasive cancer behaviours. Thus, blocking such channels in these cancers can reduce the cells' metastatic potential. Given that VGSCs are a novel therapeutic target, the aim of this thesis was to determine any potential anti-cancer effects of two VGSC-blockers, ranolazine and eleclazine, on the U87-MG adult glioblastoma cell line using a series of in vitro assays. Regarding the role of hypoxia on glioblastoma pathophysiology, it was found that lower O2 concentrations reduced proliferation but had no effect on invasiveness. Additionally, higher concentrations of eleclazine inhibited cell proliferation but ranolazine did not affect proliferative activity. Higher concentrations of eleclazine increased the number of invaded cells under both normoxia and hypoxia whereas lower concentrations only promoted invasion under hypoxia. Although higher concentrations of ranolazine had no effect on cell invasiveness, lower concentrations increased invasion under hypoxia. The results of the in vitro assays suggest that other mechanisms of ranolazine and eleclazine action may have prominent phenotypic effects on glioblastoma cells, making them unsuitable therapeutic candidates.
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