日本血凝病毒包膜包裹的微小RNA-34a-5p通过抑制生存素强烈诱导恶性脑膜瘤细胞凋亡。

Hemagglutinating virus of Japan envelope encapsulating microRNA-34a-5p robustly induces apoptosis of malignant meningioma cells by suppressing survivin.

作者信息

Ishikawa Takaaki, Matsuda Masahide, Kaneda Yasufumi, Ishikawa Eiichi

机构信息

Graduate School of Comprehensive Human Sciences, Doctoral Program in Medical Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.

Department of Neurosurgery, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.

出版信息

J Neurooncol. 2025 Jul 21. doi: 10.1007/s11060-025-05172-0.

DOI:10.1007/s11060-025-05172-0

PMID:40690186

Abstract

PURPOSE

Malignant meningiomas are characterized by high recurrence rates and limited therapeutic options beyond surgery and radiation. This study aimed to develop a novel nucleic acid-based therapeutic approach for malignant meningiomas and to evaluate its efficacy both in vitro and in vivo.

METHODS

IOMM-Lee and HKBMM cell lines were used as models of malignant meningioma. Inhibitory effects of hemagglutinating virus of Japan envelope (HVJ-E) and microRNA-34a-5p (miR-34a-5p) were assessed using cell viability assays, apoptosis assays, RT-qPCR, and western blotting. Finally, the tumor suppressive effect of HVJ-E encapsulating miR-34a-5p was evaluated using a subcutaneous xenograft model in nude mice.

RESULT

HVJ-E significantly reduced viability of malignant meningioma cells. Furthermore, HVJ-E encapsulating miR-34a-5p demonstrated enhanced anti-tumor activity by inducing apoptosis through downregulation of survivin expression. This tumor-suppressive effect was also confirmed in a subcutaneous mouse model.

CONCLUSION

Our findings indicate that HVJ-E encapsulating miR-34a-5p effectively inhibits the growth of malignant meningioma cells both in vitro and in vivo. This novel combination therapy holds promise as a potential treatment strategy for malignant meningiomas.

摘要