In brain tumors, cluster of differentiation (CD) 133 expression isĬonsidered a marker of stem cells ( 12, 13)Īnd is increased in GBM cell lines grown as spheres, compared withĮvidence that GBM tumors may originate from CSCs that are present ![]() May be associated with chemo- and radioresistance ( 9– 11). The existence of cancer stem cells (CSCs) in tumors Lines ( 5, 6), including GBM cells exposed to TP53 status affects transcriptional profiles in tumor cell Genetic heterogeneity is characteristic of GBMīackground, mutations in TP53 have been detected in 31% of Is 12–15 months following diagnosis, despite surgical resection, Patients diagnosed annually in Europe ( 1). Type of malignant brain tumor in adults, with 3.6 cases per 100,000 Glioblastoma multiforme (GBM) is the most common HEB may be a potential target to decrease proliferation in U87MG GBM cells, grown as monolayers or neurospheres, and may provide important information for the development of novel strategies for cancer therapy. However, only limited effects were exerted by irradiation in HEB‑silenced cells. These results suggest that HEB may contribute to the proliferation and maintenance of GBM cells. Differentiation of U87MG cells from neurospheres was reduced in HEB‑silenced cells, whereas in irradiated cells the proportion of CD133+ cells was similar in HEB‑silenced cells compared with the SCR control. HEB silencing combined with irradiation reduced U87MG cell proliferation when cultured in monolayers and reduced neurosphere cell number compared with the SCR irradiated group however, not significantly. In addition, HEB silencing reduced (two‑fold) the number of neurospheres compared with control scrambled (SCR) cells. HEB silencing in cells grown in monolayers induced a significant reduction in proliferation and decreased the proportion of cells in G0/G1 phase. Greater HEB protein expression was observed in U87MG neurospheres compared with ACBRI‑371, and the two cell lines exhibited nuclear HEB expression. ![]() Cell proliferation and death, cell cycle and sub‑G1 detection, and cluster of differentiation (CD) 133 immunofluorescence were analyzed by flow cytometry, whereas HEB protein expression was analyzed by immunocytochemistry and western blotting. U87MG GBM and ACBRI‑371 primary human astrocytes were cultured in monolayers or neurospheres. ![]() The present study aimed to determine whether HEB knockdown, with or without irradiation, may sensitize GBM cells. Transcription factor 12 (HEB) has been associated with neural and stem cell proliferation, is overexpressed in certain tumor types and is induced in irradiated U87MG cells. Glioblastoma multiforme (GBM) is a lethal tumor and novel strategies are required to overcome resistance.
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