RSL1D1 regulates lung adenocarcinoma progression by inhibiting NRF2 ubiquitination

被引：0

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
]}

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

来源：

GENE | 2025年 / 964卷

关键词：

NRF2; Lung adenocarcinoma progression; Ubiquitin; CANCER; PROLIFERATION;

D O I：

10.1016/j.gene.2025.149637

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

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.

引用

页数：10

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