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缺氧诱导的LGALS8-AS1维持氧化酸化以推动乳腺癌的进展

Huaying Xie¹, Di Zhou¹, Zihao Xu²

¹Department of Radiotherapy and Oncology, The Second Affiliated Hospital of Soochow University, Institute of Radiotherapy and Oncology, Soochow University, Suzhou, 215004, China; Department of Radiation Oncology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, No.160 Pujian Road, Shanghai, 200127, China.

Biochemical and biophysical research communications

|February 24, 2026

概括

这项研究确定LGALS8-AS1,一种低氧诱导的长非编码RNA,是乳腺癌进展的关键驱动因素. 它维持氧化酸化 (OXPHOS),促进瘤生长和转移.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
癌症新陈代谢癌症新陈代谢

背景情况:

缺氧是乳腺癌的一个关键因素,影响瘤的进展和代谢适应.
低氧反应的长非编码RNAs (lncRNAs) 在乳腺癌中的线粒体代谢中的作用尚不清楚.

研究的目的:

研究缺氧诱导的lncRNAs在乳腺癌中调节线粒体代谢中的功能.
确定参与低氧驱动的代谢重编程的特定lncRNA及其对瘤进展的影响.

主要方法:

在缺氧条件下对乳腺癌细胞 (T47D,MCF7) 进行转录基因分析.
通过使用遗传和记者测定来研究LGALS8-AS1通过缺氧诱导因子-1α (HIF-1α) 的转录调节.
在体内研究涉及基因删除和重新表达LGALS8-AS1在小鼠模型.
对TCGA-BRCA队列数据的分析,以将LGALS8-AS1表达与代谢途径相关联.
评估线粒体呼吸能力和呼吸链组件的表达.
评估OXPHOS抑制对瘤生长和入侵的影响.

主要成果:

鉴定出LGALS8-AS1是一种在乳腺癌细胞中上调的缺氧诱导 lncRNA.
LGALS8-AS1通过HIF-1α进行转录调节.
在体内,LGALS8-AS1的丧失抑制了瘤生长和转移,而其重新表达恢复了这些表型.
高LGALS8-AS1表达与乳腺癌患者的氧化酸化 (OXPHOS) 途径激活密切相关.
在低氧状态下,LGALS8-AS1缺乏会损害线粒体呼吸,并减少呼吸链的关键组成部分 (复合I,IV).
抑制OXPHOS可以抵消LGALS8-AS1.1.的促瘤效应.

结论:

LGALS8-AS1作为一个对缺氧反应的lncRNA,促进乳腺癌的进展.
LGALS8-AS1维持氧化酸化,将低氧信号与线粒体功能联系起来.
准LGALS8-AS1或OXPHOS可能代表乳腺癌的治疗策略.

关键词:

乳腺癌乳腺癌乳腺癌氧气过低是因为缺氧.在LGALS8-AS1中,线粒体呼吸线粒体呼吸氧化酸化是一种氧化酸化.

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