Ragazzini Gregorio, Mescola Andrea, Tassinari Riccardo, Gallerani Alessia, Zannini Chiara, Di Rosa Domenico, Cavallini Claudia, Marcuzzi Martina, Taglioli Valentina, Bighi Beatrice, Ettari Roberta, Zappavigna Vincenzo, Ventura Carlo, Alessandrini Andrea, Corsi Lorenzo
Department of Physics, Informatics and Mathematics, University of Modena and Reggio Emilia, Via Campi 213/A, 41125 Modena, Italy.
Eldor Lab, Via di Corticella 183, 40128 Bologna, Italy.
Int J Mol Sci. 2025 Mar 19;26(6):2767. doi: 10.3390/ijms26062767.
Glioblastoma multiforme (grade IV glioma) is characterized by a high invasive potential, making surgical intervention extremely challenging and patient survival very limited. Current pharmacological approaches show, at best, slight improvements in the therapy against this type of tumor. Microtubules are often the target of antitumoral drugs, and specific drugs affecting their dynamics by acting on microtubule-associated proteins (MAPs) without producing their depolymerization could affect both glioma cell migration/invasion and cell proliferation. Here, we analyzed on a cellular model of glioblastoma multiforme, the effect of a molecule (1-(4-amino-3,5-dimethylphenyl)-3,5-dihydro-7,8-ethylenedioxy-4h2,3-benzodiazepin-4-one, hereafter named 1g) which was shown to act as a cytostatic drug in other cell types by affecting microtubule dynamics. We found that the molecule acts also as a migration suppressor by inducing a loss of cell polarity. We characterized the mechanics of U87MG cell aggregates exposed to 1g by different biophysical techniques. We considered both 3D aggregates and 2D cell cultures, testing substrates of different stiffness. We established that this molecule produces a decrease of cell spheroid contractility and it impairs 3D cell invasion. At the same time, in the case of isolated cells, 1g selectively produces an almost instantaneous loss of cell polarity blocking migration and it also produces a disorganization of the mitotic spindle when cells reach mitosis, leading to frequent mitotic slippage events followed by cell death. We can state that the studied molecule produces similar effects to other molecules that are known to affect the dynamics of microtubules, but probably indirectly via microtubule-associated proteins (MAPs) and following different biochemical pathways. Consistently, we report evidence that, regarding its effect on cell morphology, this molecule shows a specificity for some cell types such as glioma cells. Interestingly, being a molecule derived from a benzodiazepine, the 1g chemical structure could allow this molecule to easily cross the blood-brain barrier. Thanks to its chemical/physical properties, the studied molecule could be a promising new drug for the specific treatment of GBM.
多形性胶质母细胞瘤(IV级胶质瘤)的特点是具有高度侵袭性,这使得手术干预极具挑战性,患者生存期也非常有限。目前的药理学方法在治疗这类肿瘤方面充其量只能带来轻微改善。微管通常是抗肿瘤药物的作用靶点,通过作用于微管相关蛋白(MAPs)而不使其解聚来影响微管动力学的特定药物,可能会影响胶质瘤细胞的迁移/侵袭以及细胞增殖。在此,我们在多形性胶质母细胞瘤的细胞模型上分析了一种分子(1 - (4 - 氨基 - 3,5 - 二甲基苯基) - 3,5 - 二氢 - 7,8 - 亚乙基二氧基 - 4H - 2,3 - 苯并二氮杂䓬 - 4 - 酮,以下简称1g)的作用,该分子在其他细胞类型中通过影响微管动力学表现出细胞生长抑制作用。我们发现该分子还通过诱导细胞极性丧失起到迁移抑制作用。我们通过不同的生物物理技术对暴露于1g的U87MG细胞聚集体的力学特性进行了表征。我们同时考虑了三维聚集体和二维细胞培养,并测试了不同硬度的底物。我们确定该分子会降低细胞球体的收缩性,并损害三维细胞侵袭。同时,对于分离的细胞,1g选择性地几乎瞬间导致细胞极性丧失从而阻止迁移,并且当细胞进入有丝分裂时还会导致有丝分裂纺锤体紊乱,引发频繁的有丝分裂滑脱事件,随后细胞死亡。我们可以说,所研究的分子产生的效果与其他已知影响微管动力学的分子类似,但可能是通过微管相关蛋白(MAPs)间接产生的,且遵循不同的生化途径。一致地,我们报告了证据表明,就其对细胞形态的影响而言,该分子对某些细胞类型如胶质瘤细胞具有特异性。有趣的是,作为一种源自苯并二氮杂䓬的分子,1g的化学结构可能使其能够轻松穿过血脑屏障。由于其化学/物理性质,所研究的分子可能是一种有前景的用于特异性治疗胶质母细胞瘤的新药。