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Hsa_circ_0004872 mitigates proliferation, metastasis and immune escape of meningioma cells by suppressing PD-L1.
Chen, Kuo; Huang, Zhengming; Liu, Changsheng; Ouyang, Qian; Yan, Qing; Zheng, Wei; Huang, Yongkai.
Afiliación
  • Chen K; Graduate Collaborative Training Base of Zhuzhou Central Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan Province, People's Republic of China.
  • Huang Z; School of Automation, Central South University, 410083, Changsha, Hunan Province, People's Republic of China.
  • Liu C; Neurosurgery Department, Zhuzhou Hospital affiliated to Xiangya Medical College of Central South University, No.116, South Changjiang Road, Tianyuan District, 412000, Zhuzhou City, Hunan Province, People's Republic of China.
  • Ouyang Q; Neurosurgery Department, Zhuzhou Hospital affiliated to Xiangya Medical College of Central South University, No.116, South Changjiang Road, Tianyuan District, 412000, Zhuzhou City, Hunan Province, People's Republic of China.
  • Yan Q; Neurosurgery Department, Zhuzhou Hospital affiliated to Xiangya Medical College of Central South University, No.116, South Changjiang Road, Tianyuan District, 412000, Zhuzhou City, Hunan Province, People's Republic of China.
  • Zheng W; Neurosurgery Department, Zhuzhou Hospital affiliated to Xiangya Medical College of Central South University, No.116, South Changjiang Road, Tianyuan District, 412000, Zhuzhou City, Hunan Province, People's Republic of China.
  • Huang Y; Neurosurgery Department, Zhuzhou Hospital affiliated to Xiangya Medical College of Central South University, No.116, South Changjiang Road, Tianyuan District, 412000, Zhuzhou City, Hunan Province, People's Republic of China. huangyk2011@163.com.
Metab Brain Dis ; 39(5): 895-907, 2024 Jun.
Article en En | MEDLINE | ID: mdl-38771413
ABSTRACT
Meningioma is a prevalent intracranial malignancy known for its aggressive growthCircular RNAs (circRNAs) play a crucial role in the development of various cancers. However, their involvement in meningioma remains understudied. This study aimed to investigate the function and underlying mechanism of hsa_circ_0004872 in meningioma. The molecular expression of hsa_circ_0004872, PD-L1 and EIF4A3 was identified by RT-qPCR and/or western blot assays. Cell viability, migration, and invasion were assessed through CCK-8 and Transwell assays, respectively. Cytotoxicity was determined using an LDH assay, and cell apoptosis was monitored by flow cytometry. The RNA and protein interactions were assessed through RNA-protein immunoprecipitation (RIP) and RNA pull down analyses. Our findings revealed that hsa_circ_0004872 expression was significantly downregulated in both meningioma tissue samples and cells. Overexpression of hsa_circ_0004872 inhibited the proliferation, metastasis, and immune escape of meningioma cells, as well as enhanced the cytotoxicity of CD8+ T cells by suppressing PD-L1. Furthermore, hsa_circ_0004872 directly interacted with EIF4A3, leading to the degradation of PD-L1 mRNA. Finally, inhibiting EIF4A3 improved the proliferation, metastasis, and immune escape of meningioma cells, as well as the cytotoxicity of CD8+ T cells. Our study demonstrated that hsa_circ_0004872 mitigated the proliferation, metastasis,and immune escape of meningioma cells by targeting the EIF4A3/PD-L1 axis. These findings suggested that hsa_circ_0004872 and EIF4A3 might serve as promising biological markers and therapeutic targets for meningioma treatment.
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Factor 4A Eucariótico de Iniciación / Proliferación Celular / Antígeno B7-H1 / ARN Circular / Neoplasias Meníngeas / Meningioma Límite: Humans Idioma: En Revista: Metab Brain Dis Asunto de la revista: CEREBRO / METABOLISMO Año: 2024 Tipo del documento: Article

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Factor 4A Eucariótico de Iniciación / Proliferación Celular / Antígeno B7-H1 / ARN Circular / Neoplasias Meníngeas / Meningioma Límite: Humans Idioma: En Revista: Metab Brain Dis Asunto de la revista: CEREBRO / METABOLISMO Año: 2024 Tipo del documento: Article