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RSL1D1 regulates lung adenocarcinoma progression by inhibiting NRF2 ubiquitination

文献类型: 外文期刊

作者: Yang, Qingzhu 1 ; Zhang, Chunyun 1 ; Zhang, Hang 2 ; Sun, Shuo 1 ; Zhao, Guibin 2 ; Yang, Qiaoyi 1 ; Huang, Xin 1 ; Yan, Endian 1 ; Li, Huaiyong 4 ; Liu, He 3 ; Zhang, Wei Wei 1 ;

作者机构: 1.Qiqihar Univ, Coll Life Sci & Agr Forestry, Qiqihar 161006, Peoples R China

2.Harbin Med Univ, Affiliated Hosp 4, Dept Thorac Surg, Harbin 150001, Peoples R China

3.Chinese Acad Trop Agr Sci, Environm & Plant Protect Inst, Haikou 571101, Peoples R China

4.First Hosp Qiqihar, Dept Chemoradiotherapy, Qiqihar 161000, Peoples R China

关键词: NRF2; Lung adenocarcinoma progression; Ubiquitin

期刊名称:GENE ( 影响因子:2.4; 五年影响因子:2.8 )

ISSN: 0378-1119

年卷期: 2025 年 964 卷

页码:

收录情况: SCI

摘要: RSL1D1, a member of the universal ribosomal protein uL1 family, plays a crucial role in various cellular processes. However, its involvement in cancer, particularly lung adenocarcinoma (LUAD), remains poorly understood. Our study reveals that RSL1D1 expression is significantly upregulated in LUAD and high levels of RSL1D1 are associated with poorer survival outcomes in LUAD patients. Functionally, RSL1D1 promotes LUAD cell proliferation by inhibiting NRF2 degradation. Intriguingly, RSL1D1 interacts with NRF2 and hinders its ubiquitination. These findings highlight the pivotal role of the RSL1D1/NRF2 regulatory axis in LUAD tumor progression, presenting a novel potential target for LUAD therapy.

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