Key result
Higher BMAL1 expression linked to increased microvascular density, peritumoral edema, and angiogenesis in human glioma.
Why the study?
The rhythm gene BMAL1 may play an important role in glioma tolerance for anti-angiogenesis therapy.
BMAL1 regulates angiogenesis and peritumoral edema in glioma via the HIF-1a/VEGF/ANG2 pathway, suggesting a potential role in anti-angiogenic therapy resistance.
May support BMAL1 as anti-angiogenic target in glioma; leaves open clinical efficacy pending human trials.
The rhythm gene BMAL1 (Brain and Muscle ARNT-Like 1) may play an important role in glioma tolerance for anti-angiogenesis therapy. In humans with glioma of different pathological grades, BMAL1 expression was significantly different, and the expression of ANG2 (Angiopoietin 2) and VEGF (Vascular endothelial growth factor) was positively correlated with the expression of BMAL1. Additionally, BMAL1 expression is positively correlated with the microvascular density and peritumoral edema of glioma. According to in vitro experiments, silencing the expression of BMAL1 in primary glioma cells results in a decrease in the expression of VEGF. In contrast, overexpression of BMAL1 promotes the expression of ANG2 and VEGF via HIF-1a pathway. Therefore, BMAL1 likely participates in the angiogenesis of glioma by modulating ANG2 and VEGF expression, alters the therapeutic effect of anti-angiogenic treatments, and promotes peritumoral brain edema of glioma.
No takes yet. Share an insight, caveat, or question.
Wang et al. (2021) studied Glioma. BMAL1 expression was evaluated on Expression of ANG2 and VEGF, microvascular density, and peritumoral edema. BMAL1 expression is positively correlated with microvascular density, peritumoral edema, and the expression of ANG2 and VEGF in human glioma, likely participating in angiogenesis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: