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源自M2巨细胞外体的Apoc1通过抑制ACSF2二氧化化,促进骨髓瘤中铁亡的抗性

Ping Yin1, Min Tang2, Guosheng Zhao1

  • 1Department of Blood Transfusion, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.

Molecular carcinogenesis
|July 23, 2024
PubMed
概括

通过抑制铁亡,M2巨异体 (M2-Exos) 通过抑制铁亡促进骨髓瘤 (OS) 的生长. 这通过Apoc1/ACSF2轴发生,其中M2-Exos中的Apoc1破坏了USP40与ACSF2的结合,促进OS细胞中的ACSF2降解和铁亡抵抗.

关键词:
在 ACSF2 的基础上.启示录的第一章.在M2巨细胞外体内,M2巨细胞外体内铁性化 (ferroptosis) 是一种骨质肉瘤 (OS) 是一种无处不在的化

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