Evidence map›Paper›PMID 39996452›Full record

ArticleCNS neuroscience & therapeutics2025

Cas9 Mouse Model of Skull Base Meningioma Driven by Combinational Gene Inactivation in Meningeal Cells.

Hailiang Tang, Feng Xu, Dan Sun, Lingyang Hua, Ji Xiong, Ming Xu, Jian Xu, Ping Zhong

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Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Hailiang TangDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.ORCID 0000-0003-1852-3128
Feng XuDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Dan SunDepartment of Operation Center, Huashan Hospital, Fudan University, Shanghai, China.
Lingyang HuaDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Ji XiongDepartment of Pathology, Huashan Hospital, Fudan University, Shanghai, China.
Ming XuDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Jian XuDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
Ping ZhongDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionNeurofibromatosis type 2 (Nf2) gene inactivation is common in sporadic and Nf2-related meningioma. There is currently scant literature describing the development of an intracranial meningioma model in animals. Given the role of Nf2 and other gene inactivation in meningeal cells, we used Cas9 mice here as the background host to establish a new animal model of skull base meningioma in this study.

aimsCas9 transgenic mice were purchased from Jackson Laboratory and raised in our institution. Subsequently, meningeal cells were obtained from the Cas9 transgenic mice, cultured in medium, and passaged in vitro. We then prepared lentivirus vector pLentiCre/gRNA, which could express the elements blocking the function of four genes: Nf2, P15

resultsTwenty Cas9 transgenic mice were successfully bred. Five mice were killed so that meningeal cells could be extracted, cultured, and infected with the lentivirus vector pLentiCre/gRNA for 72 h in vitro. The gene function test showed that Nf2, P15

conclusionsThe Cas9 mouse model of skull base meningioma generated with the Nf2 genetic defect and the combinational loss of P15

Indexed as

Disease Models, AnimalGene SilencingMeningeal NeoplasmsMeningesMeningiomaSkull Base NeoplasmsAnimalsCRISPR-Cas SystemsCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16MiceMice, TransgenicNeurofibromin 2Cyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Neurofibromin 2Cas9 mouse modelNf2 geneskull base meningioma

Identifiers

PMID39996452
PMCPMC11851153

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.