ArticleJournal of cellular and molecular medicine2024
Inhibition of UBA52 induces autophagy via EMC6 to suppress hepatocellular carcinoma tumorigenesis and progression.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Article
- RNF216 as a Promising Biomarker for Prognosis, Immunotherapy, and Chemotherapy in LIHC: A Comprehensive Pan-Cancer Analysis and Experimental Validation.Journal of Cancer · 2026Article
- Novel insights into hypoxia-driven transcriptomic and epigenetic landscapes in grade 3 meningioma.Journal of translational medicine · 2025Article
- SPDL1 overexpression was associated with poor prognosis and immune status in HCC through in vitro experiment and bioinformatics analysis.Discover oncology · 2025Article
- Study on the molecular mechanism of UBA52 and BARD1 regulating hepatocellular carcinoma through the PI3 K/AKT signaling pathway.Discover oncology · 2025Article
- Changes in Protein Expression in Warmed Human Lens Epithelium Cells Using Shotgun Proteomics.Medicina (Kaunas, Lithuania) · 2025Article
- Mechanisms and Factors Influencing Resorption of Herniated Part of Lumbar Disc Herniation: Comprehensive Review.Journal of inflammation research · 2025Review
- The perspective of ceRNA regulation of circadian rhythm on choroidal neovascularization.Scientific reports · 2024Article
- Inhibition of UBA52 induces autophagy via EMC6 to suppress hepatocellular carcinoma tumorigenesis and progression.Journal of cellular and molecular medicine · 2024Article
- Targeting cell death mechanisms: the potential of autophagy and ferroptosis in hepatocellular carcinoma therapy.Frontiers in immunology · 2024Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Ubiquitin A-52 residue ribosomal protein fusion product 1 (UBA52) has a role in the occurrence and development of tumours. However, the mechanism by which UBA52 regulates hepatocellular carcinoma (HCC) tumorigenesis and progression remains poorly understood. By using the Cell Counting Kit (CCK-8), colony formation, wound healing and Transwell assays, we assessed the effects of UBA52 knockdown and overexpression on the proliferation and migration of HCC cells in vitro. By establishing subcutaneous and metastatic tumour models in nude mice, we evaluated the effects of UBA52 on HCC cell proliferation and migration in vivo. Through bioinformatic analysis of data from the Gene Expression Profiling Interactive Analysis (GEPIA) and The Cancer Genome Atlas (TCGA) databases, we discovered that UBA52 is associated with autophagy. In addition, we discovered that HCC tissues with high UBA52 expression had a poor prognosis in patients. Moreover, knockdown of UBA52 reduced HCC cell growth and metastasis both in vitro and in vivo. Mechanistically, knockdown of UBA52 induced autophagy through EMC6 in HCC cells. These findings suggest that UBA52 promoted the proliferation and migration of HCC cells through autophagy regulation via EMC6 and imply that UBA52 may be a viable novel treatment target for HCC patients.
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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.