ArticleEBioMedicine2020
PRAS40 hyperexpression promotes hepatocarcinogenesis.
Article in EBioMedicine, 2020. 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 19 papers.
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Who cites it
19 citing papers in PubMed, 50 citations in OpenAlex.
- PRAS40-driven pro-inflammatory macrophage polarization is required for inflammatory bowel disease.Cell death & disease · 2026Article
- PRAS40 enhances glycolysis by facilitating G6PI/PGK1/LDHA complex assembly in colorectal cancer.Discover oncology · 2026Article
- PRAS40 activates the IRE1α-XBP-1-mediated unfolded protein response to exacerbate colorectal cancer by enhancing ST6Gal1-dependent α-2, 6 sialylation of GRP78.Neoplasia (New York, N.Y.) · 2026Article
- Establishment of a prognostic model for hepatocellular carcinoma patients based on bioinformatics analysis and exploration of prognostic biomarker EPPK1.Scientific reports · 2026Article
- PRAS40 promotes colorectal cancer stemness by enhancing glycolysis through triggering PGK1 acetylation.Oncogenesis · 2025Article
- Salmonella typhimurium downregulates circHIPK2 expression via CeRNA mechanism to inhibit cell migration and tumorigenesis.Gut pathogens · 2025Article
- Fuelling the Fight from the Gut: Short-Chain Fatty Acids and Dexamethasone Synergise to Suppress Gastric Cancer Cells.Cancers · 2025Article
- mTOR/miR-142-3p/PRAS40 signaling cascade is critical for tuberous sclerosis complex-associated renal cystogenesis.Cellular & molecular biology letters · 2024Article
- Comprehensive DNA methylation profiling of COVID-19 and hepatocellular carcinoma to identify common pathogenesis and potential therapeutic targets.Clinical epigenetics · 2023Article
- Inferring cancer common and specific gene networks via multi-layer joint graphical model.Computational and structural biotechnology journal · 2023Article
- Regulation of the Key Epithelial Cancer Suppressor miR-124 Function by Competing Endogenous RNAs.International journal of molecular sciences · 2022Review
- TIFA promotes colorectal cancer cell proliferation in an RSK- and PRAS40-dependent manner.Cancer science · 2022Article
- METTL14-mediated mMolecular cancer · 2022Article
- PGK1 represses autophagy-mediated cell death to promote the proliferation of liver cancer cells by phosphorylating PRAS40.Cell death & disease · 2022Article
- Crosstalk between autophagy inhibitors and endosome-related secretory pathways: a challenge for autophagy-based treatment of solid cancers.Molecular cancer · 2021Review
- The potential role of miR-124-3p in tumorigenesis and other related diseases.Molecular biology reports · 2021Review
- Machine-Learning-Based m5C Score for the Prognosis Diagnosis of Osteosarcoma.Journal of oncology · 2021Article
- Long Noncoding RNA LINC01134 Promotes Hepatocellular Carcinoma Metastasis via Activating AKT1S1 and NF-κB Signaling.Frontiers in cell and developmental biology · 2020Article
- WIPF1 regulates stemness in small cell lung cancer.Science progressArticle
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocellular carcinoma (HCC) is one of the most common cancers, whereas the molecular mechanism remains largely unknown. PRAS40 (encoded by AKT1S1) phosphorylation was increased in human melanoma, prostate cancer and lung cancer specimens, which was considered as the results of Akt activation. However the mechanism in detail and its role in HCC stay elusive.
methodsPRAS40 expression and phosphorylation were analyzed in HCC specimens, and the survival rates of patients were investigated. Functional analyses of PRAS40 in HCC were performed in vivo and in vitro. The miR-124-3p binding sites in PRAS40 were investigated using luciferase assay. MiR-124-3p expression in HCC specimens was examined by In Situ hybridization, and the correlation to PRAS40 level was evaluated.
findingsThe phosphorylation, protein and mRNA levels of PRAS40 were increased significantly in HCC specimens from our cohorts and TCGA database, which was positively correlated to the poor prognosis of HCC patients. Compared to Akt1s1
interpretationPRAS40 hyperexpression induced by loss of miR-124-3p contributes to PRAS40 hyperphosphorylation and hepatocarcinogenesis. These results could be expected to offer novel clues for understanding hepatocarcinogenesis and developing approaches.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.