Dixon Sashana, O'connor Ann Tenneil, Brooks-Noreiga Chloe, Clark Michelle A, Levy Arkene, Castejon Ana M
Barry and Judy Silverman College of Pharmacy, Nova Southeastern University, Ft. Lauderdale, FL, USA.
Halmos College of Arts and Sciences, Nova Southeastern University, Ft. Lauderdale, FL, USA.
Cancer Chemother Pharmacol. 2024 Jul;94(1):1-23. doi: 10.1007/s00280-024-04686-0. Epub 2024 Jun 25.
Glioblastoma multiforme (GBM) is a highly aggressive and incurable disease accounting for about 10,000 deaths in the USA each year. Despite the current treatment approach which includes surgery with chemotherapy and radiation therapy, there remains a high prevalence of recurrence. Notable improvements have been observed in persons receiving concurrent antihypertensive drugs such as renin angiotensin inhibitors (RAS) or the antidiabetic drug metformin with standard therapy. Anti-tumoral effects of RAS inhibitors and metformin have been observed in in vitro and in vivo studies. Although clinical trials have shown mixed results, the potential for the use of RAS inhibitors and metformin as adjuvant GBM therapy remains promising. Nevertheless, evidence suggest that these drugs exert multimodal antitumor actions; by particularly targeting several cancer hallmarks. In this review, we highlight the results of clinical studies using multidrug cocktails containing RAS inhibitors and or metformin added to standard therapy for GBM. In addition, we highlight the possible molecular mechanisms by which these repurposed drugs with an excellent safety profile might elicit their anti-tumoral effects. RAS inhibition elicits anti-inflammatory, anti-angiogenic, and immune sensitivity effects in GBM. However, metformin promotes anti-migratory, anti-proliferative and pro-apoptotic effects mainly through the activation of AMP-activated protein kinase. Also, we discussed metformin's potential in targeting both GBM cells as well as GBM associated-stem cells. Finally, we summarize a few drug interactions that may cause an additive or antagonistic effect that may lead to adverse effects and influence treatment outcome.
多形性胶质母细胞瘤(GBM)是一种极具侵袭性且无法治愈的疾病,在美国每年约导致10000人死亡。尽管目前的治疗方法包括手术、化疗和放疗,但复发率仍然很高。在接受肾素血管紧张素抑制剂(RAS)等联合抗高血压药物或抗糖尿病药物二甲双胍与标准治疗的患者中,已观察到显著改善。在体外和体内研究中均观察到RAS抑制剂和二甲双胍的抗肿瘤作用。尽管临床试验结果不一,但将RAS抑制剂和二甲双胍用作GBM辅助治疗的潜力仍然很大。然而,有证据表明这些药物具有多模式抗肿瘤作用;特别是针对几个癌症特征。在本综述中,我们重点介绍了使用含有RAS抑制剂和/或二甲双胍的多药鸡尾酒添加到GBM标准治疗中的临床研究结果。此外,我们强调了这些具有良好安全性的重新利用药物可能引发其抗肿瘤作用的可能分子机制。RAS抑制在GBM中引发抗炎、抗血管生成和免疫敏感作用。然而,二甲双胍主要通过激活AMP激活的蛋白激酶促进抗迁移、抗增殖和促凋亡作用。此外,我们还讨论了二甲双胍在靶向GBM细胞以及GBM相关干细胞方面的潜力。最后,我们总结了一些可能导致相加或拮抗作用的药物相互作用,这些作用可能导致不良反应并影响治疗结果。