Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma
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 an...
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Format: | Article |
Language: | English |
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Nature Publishing Group
2022-08-01
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Series: | Cell Death Discovery |
Online Access: | https://doi.org/10.1038/s41420-022-01153-8 |
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author | Dongmei Zhang Yunzhen Zhou Yanan Ma Ping Jiang Hongchao Lv Sijia Liu Yu Mu Chong Zhou Shan Xiao Guohua Ji Peng Liu Ning Zhang Donglin Sun Haiming Sun Nan Wu Yan Jin |
author_facet | Dongmei Zhang Yunzhen Zhou Yanan Ma Ping Jiang Hongchao Lv Sijia Liu Yu Mu Chong Zhou Shan Xiao Guohua Ji Peng Liu Ning Zhang Donglin Sun Haiming Sun Nan Wu Yan Jin |
author_sort | Dongmei Zhang |
collection | DOAJ |
description | 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. |
first_indexed | 2024-12-10T18:51:21Z |
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id | doaj.art-0057c969bcfd447a9f3fe5638ed75ecf |
institution | Directory Open Access Journal |
issn | 2058-7716 |
language | English |
last_indexed | 2024-12-10T18:51:21Z |
publishDate | 2022-08-01 |
publisher | Nature Publishing Group |
record_format | Article |
series | Cell Death Discovery |
spelling | doaj.art-0057c969bcfd447a9f3fe5638ed75ecf2022-12-22T01:37:17ZengNature Publishing GroupCell Death Discovery2058-77162022-08-01811910.1038/s41420-022-01153-8Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinomaDongmei Zhang0Yunzhen Zhou1Yanan Ma2Ping Jiang3Hongchao Lv4Sijia Liu5Yu Mu6Chong Zhou7Shan Xiao8Guohua Ji9Peng Liu10Ning Zhang11Donglin Sun12Haiming Sun13Nan Wu14Yan Jin15Laboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityCollege of Bioinformatics Science and Technology, Harbin Medical UniversityDepartment of Gynecological Radiotherapy, Harbin Medical University Cancer HospitalLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityLaboratory of Medical Genetics, Harbin Medical UniversityAbstract 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.https://doi.org/10.1038/s41420-022-01153-8 |
spellingShingle | Dongmei Zhang Yunzhen Zhou Yanan Ma Ping Jiang Hongchao Lv Sijia Liu Yu Mu Chong Zhou Shan Xiao Guohua Ji Peng Liu Ning Zhang Donglin Sun Haiming Sun Nan Wu Yan Jin Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma Cell Death Discovery |
title | Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma |
title_full | Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma |
title_fullStr | Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma |
title_full_unstemmed | Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma |
title_short | Ribosomal protein L22-like1 (RPL22L1) mediates sorafenib sensitivity via ERK in hepatocellular carcinoma |
title_sort | ribosomal protein l22 like1 rpl22l1 mediates sorafenib sensitivity via erk in hepatocellular carcinoma |
url | https://doi.org/10.1038/s41420-022-01153-8 |
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