2. Academic Validation
  3. Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma

Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma

  • Cell Death Discov. 2022 Aug 17;8(1):365. doi: 10.1038/s41420-022-01153-8.
Dongmei Zhang 1 2 3,  Yunzhen Zhou 1 2,  Yanan Ma 1 2,  Ping Jiang 1 2,  Hongchao Lv 4,  Sijia Liu 5,  Yu Mu 1 2,  Chong Zhou 1 2,  Shan Xiao 1 2,  Guohua Ji 1,  Peng Liu 1,  Ning Zhang 1 2,  Donglin Sun 1 2,  Haiming Sun 1 2,  Nan Wu 6 7,  Yan Jin 8 9
Affiliations

Affiliations

  • 1 Laboratory of Medical Genetics, Harbin Medical University, Harbin, China.
  • 2 Key laboratory of preservation of human genetic resources and disease control in China (Harbin Medical University), Ministry of Education, Harbin, China.
  • 3 Department of Histology and Embryology, Harbin Medical University-Daqing, Daqing, China.
  • 4 College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
  • 5 Department of Gynecological Radiotherapy, Harbin Medical University Cancer Hospital, Harbin, China.
  • 6 Laboratory of Medical Genetics, Harbin Medical University, Harbin, China. wunan@hrbmu.edu.cn.
  • 7 Key laboratory of preservation of human genetic resources and disease control in China (Harbin Medical University), Ministry of Education, Harbin, China. wunan@hrbmu.edu.cn.
  • 8 Laboratory of Medical Genetics, Harbin Medical University, Harbin, China. jinyan@hrbmu.edu.cn.
  • 9 Key laboratory of preservation of human genetic resources and disease control in China (Harbin Medical University), Ministry of Education, Harbin, China. jinyan@hrbmu.edu.cn.
PMID: 35973992 DOI: 10.1038/s41420-022-01153-8
Abstract

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.

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