Vancsik Tamás, Máthé Domokos, Horváth Ildikó, Várallyaly Anett Anna, Benedek Anett, Bergmann Ralf, Krenács Tibor, Benyó Zoltán, Balogh Andrea
1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.
Department of Biophysics and Radiation Biology, Semmelweis University, Budapest, Hungary.
Front Oncol. 2021 Feb 25;11:590764. doi: 10.3389/fonc.2021.590764. eCollection 2021.
Modulated electro-hyperthermia (mEHT), induced by 13.56 MHz radiofrequency, has been demonstrated both in preclinical and clinical studies to efficiently induce tumor damage and complement other treatment modalities. Here, we used a mouse xenograft model of human melanoma (A2058) to test mEHT (~42°C) both alone and combined with NK-cell immunotherapy. A single 30 min shot of mEHT resulted in significant tumor damage due to induced stress, marked by high hsp70 expression followed by significant upregulation of cleaved/activated caspase-3 and p53. When mEHT was combined with either primary human NK cells or the IL-2 independent NK-92MI cell line injected subcutaneously, the accumulation of NK cells was observed at the mEHT pretreated melanoma nodules but not at the untreated controls. mEHT induced the upregulation of the chemoattractant CXCL11 and increased the expression of the matrix metalloproteinase MMP2 which could account for the NK-cell attraction into the treated melanoma. In conclusion, mEHT monotherapy of melanoma xenograft tumors induced irreversible heat and cell stress leading to caspase dependent apoptosis to be driven by p53. mEHT could support the intratumoral attraction of distantly injected NK-cells, contributed by CXCL11 and MMP2 upregulation, resulting in an additive tumor destruction and growth inhibition. Therefore, mEHT may offer itself as a good partner for immunotherapy.
由13.56兆赫射频诱导的调制式电超高温疗法(mEHT),在临床前和临床研究中均已证明能有效诱导肿瘤损伤并补充其他治疗方式。在此,我们使用人黑色素瘤(A2058)的小鼠异种移植模型来单独测试mEHT(约42°C)以及将其与自然杀伤细胞(NK细胞)免疫疗法联合使用。单次30分钟的mEHT治疗因诱导应激导致显著的肿瘤损伤,其特征为热休克蛋白70(hsp70)高表达,随后裂解/活化的半胱天冬酶-3(caspase-3)和p53显著上调。当mEHT与皮下注射的原代人NK细胞或白细胞介素-2非依赖性NK-92MI细胞系联合使用时,在mEHT预处理的黑色素瘤结节处观察到NK细胞的聚集,而在未处理的对照处则未观察到。mEHT诱导趋化因子CXC趋化因子配体11(CXCL11)上调,并增加基质金属蛋白酶2(MMP2)的表达,这可能是NK细胞被吸引至经治疗的黑色素瘤的原因。总之,黑色素瘤异种移植肿瘤的mEHT单一疗法诱导了不可逆的热和细胞应激,导致由p53驱动的半胱天冬酶依赖性凋亡。mEHT可支持远处注射的NK细胞在肿瘤内的吸引,这是由CXCL11和MMP2上调促成的,从而导致肿瘤破坏和生长抑制的相加作用。因此,mEHT可能是免疫疗法的良好搭档。