ArticleCancer medicine2025
RIOK1: A Novel Oncogenic Driver in Hepatocellular Carcinoma.
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The atypical kinase right open reading frame kinase 1 suppresses glioma cell growth through mammalian target of rapamycin inhibition and apoptotic signaling activation.Translational cancer research · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundHepatocellular carcinoma (HCC) is one of the most common and highly lethal cancers worldwide. RIO kinase 1 (RIOK1), a protein kinase/ATPase that plays a key role in regulating translation and ribosome assembly, is associated with a variety of malignant tumors. However, the role of RIOK1 in HCC remains largely unknown.
methodsChanges in RIOK1 expression in HCC and patient prognosis were evaluated using HCC tissues and public databases. The functional role of RIOK1 in HCC was analyzed by RTCA assay, clonogenic assay, and flow cytometry in vitro, and by mouse tumor xenograft model in vivo. Potential mechanism studies were performed using multi-omics analysis, public database screening, and qRT-PCR assay.
resultsIn this study, we found that RIOK1 was elevated in HCC tissues and correlated with poor prognosis. Functional assays demonstrated that RIOK1 knockdown suppressed HCC cell proliferation, survival, and tumor growth in vivo, while RIOK1 overexpression enhanced these oncogenic phenotypes. Meanwhile, RIOK1 knockdown affected cell cycle progression and the expression of cyclin A2 and cyclin B1. Furthermore, integrated transcriptomic and proteomic analysis revealed that RIOK1 may promote HCC cell proliferation by affecting the cell cycle and DNA repair pathways. Moreover, we identified five potential effectors regulated by RIOK1: PMS1, SPDL1, RAD18, BARD1, and SMARCA5, which were highly expressed in HCC tissues and negatively correlated with the overall survival of HCC patients.
conclusionOur findings suggest that RIOK1 is a novel oncogenic driver that may serve as a potential diagnostic and therapeutic target for HCC.
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