ArticleCancer gene therapy2023
A20 interacts with mTORC2 to inhibit the mTORC2/Akt/Rac1 signaling axis in hepatocellular carcinoma cells.
Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 4 citations in OpenAlex.
- A20 Inhibits IFN-γ Signaling in Hepatocellular Carcinoma Cells by Binding to STAT1, Compromising Anti-Tumor Immunity.Cancer science · 2026Article
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Non-coding RNAs (ncRNAs)-mediated high expression of Ras-related C3 botulinum toxin substrate 1 (RAC1) correlates with poor prognosis and tumor immune infiltration of liver hepatocellular carcinoma.Translational cancer research · 2026Article
- STOML2 promotes hepatocellular carcinoma cell proliferation, invasion and migration by activating the PI3K/AKT signaling pathway (Review).Oncology letters · 2026Review
- A novel missense variant in TNFAIP3 associated with autoimmunity reveals the contribution of STAT1/mTOR pathways.Clinical and experimental immunology · 2025Article
- Review
- Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles.Advances in experimental medicine and biology · 2023Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A20 acts as a tumor suppressor in hepatocellular carcinoma, especially inhibiting metastasis of the malignant cells. However, the mechanisms whereby A20 plays the inhibitory roles are not understood completely. Rac1 signaling is essential for cell migration in hepatocellular carcinoma metastasis. Nevertheless, it is not known whether and how A20 inhibits Rac1 signaling to suppress the migration of hepatocellular carcinoma cell. Thereby, we analyzed the relationship between A20 and Rac1 activation, as well as the activity of Akt and mTORC2, two signaling components upstream of Rac1, using gain and loss of function experiments. We found that the overexpression of A20 repressed, while the knockdown or knockout of A20 promoted, the activation of Rac1, Akt and mTORC2 in hepatocellular carcinoma cells. Moreover, the inhibitory effect of A20 on the mTORC2/Akt/Rac1 signaling axis was due to the interaction between A20 and mTORC2 complex. The binding of A20 to mTORC2 was mediated by the ZnF7 domain of A20 and M1 ubiquitin chain in the mTORC2 complex. Furthermore, A20 inhibited metastasis of hepatocellular carcinoma cells via restraining mTORC2 in a hepatocellular carcinoma xenograft mouse model. These findings revealed the relationship between A20 and mTORC2, and explained the molecular mechanisms of A20 in inhibition of hepatocellular carcinoma metastasis.
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