核糖体蛋白L22样蛋白1（RPL22L1）通过细胞外调节蛋白激酶（ERK）介导肝癌对索拉非尼的敏感性。
Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma.
作者信息
Zhang Dongmei, Zhou Yunzhen, Ma Yanan, Jiang Ping, Lv Hongchao, Liu Sijia, Mu Yu, Zhou Chong, Xiao Shan, Ji Guohua, Liu Peng, Zhang Ning, Sun Donglin, Sun Haiming, Wu Nan, Jin Yan
机构信息
Laboratory of Medical Genetics, Harbin Medical University, Harbin, China.
Key laboratory of preservation of human genetic resources and disease control in China (Harbin Medical University), Ministry of Education, Harbin, China.
出版信息
Cell Death Discov. 2022 Aug 17;8(1):365. doi: 10.1038/s41420-022-01153-8.
Precision medicine in hepatocellular carcinoma (HCC) relies on validated biomarkers that help subgroup patients for targeted treatment. Here, we identified a novel candidate oncogene, ribosomal protein L22-like1 (RPL22L1), which was markedly elevated in HCC, contributed to HCC malignancy and adverse patient survival. Functional studies indicated RPL22L1 overexpression accelerated cell proliferation, migration, invasion and sorafenib resistance. Mechanism studies revealed that RPL22L1 activated ERK to induce atypical epithelial-to-mesenchymal transition (EMT) progress. Importantly, the ERK inhibitor (ERKi) could potentiate sorafenib efficiency in RPL22L1-high HCC cells. In summary, these data uncover RPL22L1 is a potential marker to guide precision therapy for utilizing ERKi to enhance the sorafenib efficacy in RPL22L1-high HCC patients.
肝细胞癌（HCC）的精准医学依赖于经过验证的生物标志物，这些标志物有助于对患者进行亚组分类以实施靶向治疗。在此，我们鉴定出一种新型候选癌基因，核糖体蛋白L22样1（RPL22L1），其在HCC中显著升高，促进了HCC的恶性进展及患者不良生存。功能研究表明，RPL22L1过表达加速了细胞增殖、迁移、侵袭及对索拉非尼的耐药性。机制研究显示，RPL22L1激活ERK以诱导非典型上皮-间质转化（EMT）进程。重要的是，ERK抑制剂（ERKi）可增强RPL22L1高表达的HCC细胞对索拉非尼的敏感性。总之，这些数据揭示RPL22L1是一种潜在标志物，可指导精准治疗，即利用ERKi提高RPL22L1高表达的HCC患者对索拉非尼的疗效。
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