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

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

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.

Related collections

Most cited references 36

Record: found
Abstract: found
Article: not found

Hepatocellular carcinoma

Josep Llovet, Robin Kate Kelley, Augusto Villanueva … (2021)

Liver cancer remains a global health challenge, with an estimated incidence of >1 million cases by 2025. Hepatocellular carcinoma (HCC) is the most common form of liver cancer and accounts for ~90% of cases. Infection by hepatitis B virus and hepatitis C virus are the main risk factors for HCC development, although non-alcoholic steatohepatitis associated with metabolic syndrome or diabetes mellitus is becoming a more frequent risk factor in the West. Moreover, non-alcoholic steatohepatitis-associated HCC has a unique molecular pathogenesis. Approximately 25% of all HCCs present with potentially actionable mutations, which are yet to be translated into the clinical practice. Diagnosis based upon non-invasive criteria is currently challenged by the need for molecular information that requires tissue or liquid biopsies. The current major advancements have impacted the management of patients with advanced HCC. Six systemic therapies have been approved based on phase III trials (atezolizumab plus bevacizumab, sorafenib, lenvatinib, regorafenib, cabozantinib and ramucirumab) and three additional therapies have obtained accelerated FDA approval owing to evidence of efficacy. New trials are exploring combination therapies, including checkpoint inhibitors and tyrosine kinase inhibitors or anti-VEGF therapies, or even combinations of two immunotherapy regimens. The outcomes of these trials are expected to change the landscape of HCC management at all evolutionary stages.

0 comments Cited 1705 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Identification of the tumour transition states occurring during EMT

Cédric Blanpain, Ievgenia Pastushenko, Audrey Brisebarre … (2018)

In cancer, the epithelial-to-mesenchymal transition (EMT) is associated with tumour stemness, metastasis and resistance to therapy. It has recently been proposed that, rather than being a binary process, EMT occurs through distinct intermediate states. However, there is no direct in vivo evidence for this idea. Here we screen a large panel of cell surface markers in skin and mammary primary tumours, and identify the existence of multiple tumour subpopulations associated with different EMT stages: from epithelial to completely mesenchymal states, passing through intermediate hybrid states. Although all EMT subpopulations presented similar tumour-propagating cell capacity, they displayed differences in cellular plasticity, invasiveness and metastatic potential. Their transcriptional and epigenetic landscapes identify the underlying gene regulatory networks, transcription factors and signalling pathways that control these different EMT transition states. Finally, these tumour subpopulations are localized in different niches that differentially regulate EMT transition states.

0 comments Cited 457 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Compromised MAPK signaling in human diseases: an update.

Eun-Kyung Kim, Eui-Ju Choi (2015)

The mitogen-activated protein kinases (MAPKs) in mammals include c-Jun NH2-terminal kinase (JNK), p38 MAPK, and extracellular signal-regulated kinase (ERK). These enzymes are serine-threonine protein kinases that regulate various cellular activities including proliferation, differentiation, apoptosis or survival, inflammation, and innate immunity. The compromised MAPK signaling pathways contribute to the pathology of diverse human diseases including cancer and neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. The JNK and p38 MAPK signaling pathways are activated by various types of cellular stress such as oxidative, genotoxic, and osmotic stress as well as by proinflammatory cytokines such as tumor necrosis factor-α and interleukin 1β. The Ras-Raf-MEK-ERK signaling pathway plays a key role in cancer development through the stimulation of cell proliferation and metastasis. The p38 MAPK pathway contributes to neuroinflammation mediated by glial cells including microglia and astrocytes, and it has also been associated with anticancer drug resistance in colon and liver cancer. We here summarize recent research on the roles of MAPK signaling pathways in human diseases, with a focus on cancer and neurodegenerative conditions.

0 comments Cited 389 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Nan Wu:

ORCID: http://orcid.org/0000-0002-7401-4136

wunan@hrbmu.edu.cn

Yan Jin:

ORCID: http://orcid.org/0000-0001-6282-7095

jinyan@hrbmu.edu.cn

Journal

Journal ID (nlm-ta): Cell Death Discov

Journal ID (iso-abbrev): Cell Death Discov

Title: Cell Death Discovery

Publisher: Nature Publishing Group UK (London )

ISSN (Electronic): 2058-7716

Publication date (Electronic): 17 August 2022

Publication date PMC-release: 17 August 2022

Publication date Collection: 2022

Volume: 8

Electronic Location Identifier: 365

Affiliations

[1 ]GRID grid.410736.7, ISNI 0000 0001 2204 9268, Laboratory of Medical Genetics, , Harbin Medical University, ; Harbin, China

[2 ]GRID grid.419897.a, ISNI 0000 0004 0369 313X, Key laboratory of preservation of human genetic resources and disease control in China (Harbin Medical University), Ministry of Education, ; Harbin, China

[3 ]GRID grid.410736.7, ISNI 0000 0001 2204 9268, Department of Histology and Embryology, , Harbin Medical University-Daqing, ; Daqing, China

[4 ]GRID grid.410736.7, ISNI 0000 0001 2204 9268, College of Bioinformatics Science and Technology, , Harbin Medical University, ; Harbin, China

[5 ]GRID grid.412651.5, ISNI 0000 0004 1808 3502, Department of Gynecological Radiotherapy, , Harbin Medical University Cancer Hospital, ; Harbin, China

Author information

Nan Wu http://orcid.org/0000-0002-7401-4136

Yan Jin http://orcid.org/0000-0001-6282-7095

Article

Publisher ID: 1153

DOI: 10.1038/s41420-022-01153-8

PMC ID: 9381560

PubMed ID: 35973992

SO-VID: a329af4f-d346-42da-9100-8440087aedac

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 18 May 2022

Date revision received : 23 July 2022

Date accepted : 27 July 2022

Funding

Funded by: FundRef https://doi.org/10.13039/501100001809, National Natural Science Foundation of China (National Science Foundation of China);

Award ID: 81871415

Award ID: 82172353

Award Recipient : Yan Jin

Funded by: FundRef https://doi.org/10.13039/100012548, Heilongjiang Postdoctoral Science Foundation;

Award ID: LBH-TZ2020

Award Recipient : Nan Wu

Funded by: University Nursing Program for Young Scholars with Creative Talents in Heilongjiang Province (UNPYSCT-2018057)

Custom metadata

Keywords: oncogenes,tumour biomarkers,growth factor signalling

Data availability:

Keywords: oncogenes, tumour biomarkers, growth factor signalling

Comments

Comment on this article

scite_

Cited by 4

See all cited by

Most referenced authors 504

See all reference authors

- Version 1

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

Read this article at

Abstract

Related collections

Journal of Circulating Biomarkers

Most cited references 36

Hepatocellular carcinoma

Identification of the tumour transition states occurring during EMT

Compromised MAPK signaling in human diseases: an update.

Author and article information

Contributors

Journal

Affiliations

Author information

Article

History

Funding

Categories

Custom metadata

Comments

Comment on this article

Similar content 549

Cited by 4

Most referenced authors 504