Suppression of the Eag1 potassium channel sensitizes glioblastoma cells to injury caused by temozolomide

摘要: Glioblastoma multiforme (GBM) is the most aggressive type of human primary brain tumor. The standard treatment protocol includes radiotherapy in combination with temozolomide (TMZ). Despite advances GBM treatment, survival time patients diagnosed glioma 14.5 months. Regarding tumor biology, various types cancer cell overexpress ether a go-go 1 (Eag1) potassium channel. Therefore, present study examined role Eag1 damage caused by TMZ on U87MG glioblastoma line. was inhibited using channel blocker (astemizole) or silenced short-hairpin RNA expression vector (pKv10.1-3). pKv10.1-3 (0.2 µg) improved silencing 250 µM TMZ, as determined reverse transcription-quantitative polymerase chain reaction and immunocytochemistry. Additionally, inhibiting astemizole (5 µM) reduced viability sensitized cells to TMZ. Cell decreased 63% for + compared 34% alone, 77% 46% MTT assay. In addition, both increased apoptosis rate triggered an Annexin V Collectively, current data reveal that has Furthermore, suppression this can improve action cells. Thus, promising strategy merits additional studies animal models glioma.