Academic Journal

Inhibition of Radiation and Temozolomide-Induced Glioblastoma Invadopodia Activity Using Ion Channel Drugs

التفاصيل البيبلوغرافية
العنوان: Inhibition of Radiation and Temozolomide-Induced Glioblastoma Invadopodia Activity Using Ion Channel Drugs
المؤلفون: Marija Dinevska, Natalia Gazibegovic, Andrew P. Morokoff, Andrew H. Kaye, Katharine J. Drummond, Theo Mantamadiotis, Stanley S. Stylli
المصدر: Cancers; Volume 12; Issue 10; Pages: 2888
بيانات النشر: Multidisciplinary Digital Publishing Institute
سنة النشر: 2020
المجموعة: MDPI Open Access Publishing
مصطلحات موضوعية: glioma, glioblastoma, invasion, invadopodia, ion channels, drug repurposing
الوصف: Glioblastoma (GBM) is the most prevalent and malignant type of primary brain cancer. The rapid invasion and dissemination of tumor cells into the surrounding normal brain is a major driver of tumor recurrence, and long-term survival of GBM patients is extremely rare. Actin-rich cell membrane protrusions known as invadopodia can facilitate the highly invasive properties of GBM cells. Ion channels have been proposed to contribute to a pro-invasive phenotype in cancer cells and may also be involved in the invadopodia activity of GBM cells. GBM cell cytotoxicity screening of several ion channel drugs identified three drugs with potent cell killing efficacy: flunarizine dihydrochloride, econazole nitrate, and quinine hydrochloride dihydrate. These drugs demonstrated a reduction in GBM cell invadopodia activity and matrix metalloproteinase-2 (MMP-2) secretion. Importantly, the treatment of GBM cells with these drugs led to a significant reduction in radiation/temozolomide-induced invadopodia activity. The dual cytotoxic and anti-invasive efficacy of these agents merits further research into targeting ion channels to reduce GBM malignancy, with a potential for future clinical translation in combination with the standard therapy.
نوع الوثيقة: text
وصف الملف: application/pdf
اللغة: English
Relation: Cancer Therapy; https://dx.doi.org/10.3390/cancers12102888
DOI: 10.3390/cancers12102888
الاتاحة: https://doi.org/10.3390/cancers12102888
Rights: https://creativecommons.org/licenses/by/4.0/
رقم الانضمام: edsbas.A828683D
قاعدة البيانات: BASE