ArticleJournal of experimental & clinical cancer research : CR2019
Elevated TRIP13 drives the AKT/mTOR pathway to induce the progression of hepatocellular carcinoma via interacting with ACTN4.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 90 citations in OpenAlex.
- Article
- Targeting mitochondrial TRIP13-AIF interaction suppresses myeloid leukemia progression and overcomes drug resistance.Oncogene · 2026Article
- TRIP13-induced NUSAP1 upregulation promotes CcRCC progression through EMT and PI3K/AKT/mTOR pathway.Journal of translational medicine · 2025Article
- Advancing the development of TRIP13 inhibitors: A high-throughput screening approach.SLAS discovery : advancing life sciences R & D · 2025Article
- Identification and validation a novel kinase-related gene signature for predicting prognosis and responsiveness to immunotherapy in hepatocellular carcinoma.Clinical and experimental medicine · 2025Article
- Machine learning-based identification of telomere-related gene signatures for prognosis and immunotherapy response in hepatocellular carcinoma.Molecular cytogenetics · 2025Article
- Prognostic assessment of early-stage liver cirrhosis induced by HCV using an integrated model of CX3CR1-associated immune infiltration genes.Scientific reports · 2025Article
- PD-L1/ITGB4 Axis Modulates Sensitivity of Hepatocellular Carcinoma to Sorafenib via FAK/AKT/mTOR Signaling Pathway.ImmunoTargets and therapy · 2025Article
- TRIP13: A promising cancer immunotherapy target.Cancer innovation · 2024Review
- TRIP13 regulates progression of gastric cancer through stabilising the expression of DDX21.Cell death & disease · 2024Article
- TRIP13 Plays an Important Role in the Sensitivity of Leukemia Cell Response to Sulforaphane Therapy.ACS omega · 2024Article
- Systematic integration of molecular and clinical approaches in HCV-induced hepatocellular carcinoma.Journal of translational medicine · 2024Article
- Article
- The novel norcantharidin derivative DCZ5417 suppresses multiple myeloma progression by targeting the TRIP13-MAPK-YWHAE signaling pathway.Journal of translational medicine · 2023Article
- Identification of Tumor-SuppressiveCancers · 2023Article
- Targeting TRIP13 for overcoming anticancer drug resistance (Review).Oncology reports · 2023Article
- Identification of a Five Immune Term Signature for Prognosis and Therapy Options (Immunotherapy versus Targeted Therapy) for Patients with Hepatocellular Carcinoma.Computational and mathematical methods in medicine · 2023Article
- Three E2F target-related genes signature for predicting prognosis, immune features, and drug sensitivity in hepatocellular carcinoma.Frontiers in molecular biosciences · 2023Article
- Genomic profiling and the impact of MUC19 mutation in hepatoid adenocarcinoma of the stomach.Cancer communications (London, England) · 2022Article
- Four-gene signature predicting overall survival and immune infiltration in hepatocellular carcinoma by bioinformatics analysis with RT‒qPCR validation.BMC cancer · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundATPase associated with a variety of cellular activities (AAA ATPase) family members are closely linked to tumor formation and progression. However, their roles in hepatocellular carcinoma (HCC) largely remain unclear.
methodsBioinformatic analyses of public databases were used to excavate the potential AAA ATPases that may contribute to HCC, and thyroid hormone receptor interactor 13 (TRIP13) was selected to following researches because of its most prominently differential expression. Western blot, qRT-PCR and immunohistochemistry were used to detect the expression of TRIP13 in HCC tissues, and then the relationship between TRIP13 expression and clinicopathological parameters were evaluated. Finally, its functions and potential mechanisms were investigated through a series gain- and loss-of-function strategies both in vitro and in vivo.
resultsTRIP13 was significantly overexpressed in HCC tissues and high level of TRIP13 was closely correlated with a worse clinical outcome. Functionally, elevated TRIP13 facilitated cell proliferation, migration, invasion, and promoted cellular epithelial-mesenchymal transition (EMT) in vitro, while promote tumor growth and lung metastasis in vivo. Mechanistically, TRIP13 interacted with ACTN4 and positively regulated its expression, thus activating the AKT/mTOR pathway to drive tumor progression. Moreover, miR-192-5p served as an upstream regulator of TRIP13 by directly binding to TRIP13 mRNA 3' UTR, which may partially explain the high expression of TRIP13 in HCC.
conclusionOur findings identified TRIP13 as a promising candidate oncogene in HCC, and TRIP13 induced cell migration, invasion and metastasis of HCC through the AKT/mTOR signaling via interacting with ACTN4.
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