Department of Biomedical Sciences, University of Padova, 35131 Padova, Italy.
Institute of Neuroscience, National Research Council (CNR), 35131 Padova, Italy.
Cells. 2024 Jul 8;13(13):1162. doi: 10.3390/cells13131162.
Malignant Peripheral Nerve Sheath Tumors (MPNSTs) are aggressive sarcomas that can arise both sporadically and in patients with the genetic syndrome Neurofibromatosis type 1 (NF1). Prognosis is dismal, as large dimensions, risk of relapse, and anatomical localization make surgery poorly effective, and no therapy is known. Hence, the identification of MPNST molecular features that could be hit in an efficient and selective way is mandatory to envision treatment options. Here, we find that MPNSTs express high levels of the glycolytic enzyme Hexokinase 2 (HK2), which is known to shield cancer cells from noxious stimuli when it localizes at MAMs (mitochondria-associated membranes), contact sites between mitochondria and endoplasmic reticulum. A HK2-targeting peptide that dislodges HK2 from MAMs rapidly induces a massive death of MPNST cells. After identifying different matrix metalloproteases (MMPs) expressed in the MPNST microenvironment, we have designed HK2-targeting peptide variants that harbor cleavage sites for these MMPs, making such peptides activatable in the proximity of cancer cells. We find that the peptide carrying the MMP2/9 cleavage site is the most effective, both in inhibiting the in vitro tumorigenicity of MPNST cells and in hampering their growth in mice. Our data indicate that detaching HK2 from MAMs could pave the way for a novel anti-MPNST therapeutic strategy, which could be flexibly adapted to the protease expression features of the tumor microenvironment.
恶性外周神经鞘瘤(MPNST)是一种侵袭性肉瘤,可在散发性和神经纤维瘤病 1 型(NF1)患者中发生。由于大尺寸、复发风险和解剖定位使手术效果不佳,且尚无已知的治疗方法,因此预后较差。因此,必须确定 MPNST 的分子特征,以便以有效和选择性的方式对其进行靶向治疗,从而为治疗方案提供思路。在这里,我们发现 MPNST 表达高水平的糖酵解酶己糖激酶 2(HK2),当它定位于线粒体相关膜(MAMs),即线粒体和内质网之间的接触点时,HK2 可保护癌细胞免受有害刺激。一种可将 HK2 从 MAMs 上置换下来的 HK2 靶向肽可迅速诱导 MPNST 细胞大量死亡。在鉴定出 MPNST 微环境中表达的不同基质金属蛋白酶(MMPs)后,我们设计了携带这些 MMP 切割位点的 HK2 靶向肽变体,使这些肽在靠近癌细胞的地方具有活性。我们发现携带 MMP2/9 切割位点的肽最有效,既能抑制 MPNST 细胞的体外致瘤性,又能阻止其在小鼠体内的生长。我们的数据表明,将 HK2 从 MAMs 上分离下来可能为一种新的抗 MPNST 治疗策略铺平道路,该策略可根据肿瘤微环境中蛋白酶的表达特征进行灵活调整。