ArticleCell death & disease2018
TRIM50 suppressed hepatocarcinoma progression through directly targeting SNAIL for ubiquitous degradation.
Article in Cell death & disease, 2018. 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 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Regulatory mechanisms for Snail protein stability: ubiquitin-proteasome system and chaperone-mediated autophagy.Experimental & molecular medicine · 2026Review
- MPP7 inhibits tumor metastasis through promoting snail degradation in clear cell renal cell carcinoma.Cellular & molecular biology letters · 2026Article
- Ubiquitination mediated by RING-type E3 ligases in the progression of digestive system tumors: mechanistic insights and potential therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- TRIM68 regulates ubiquitinated degradation of Rabex-5 and plays a role in progression of breast cancer through Rab5-Rac1.American journal of cancer research · 2026Article
- Unraveling the anoikis-cancer nexus: a bibliometric analysis of research trends and mechanisms.Future science OA · 2025Article
- MAZ-mediated N6-methyladenosine modification of ZEB1 promotes hepatocellular carcinoma progression by regulating METTL3.Journal of translational medicine · 2025Article
- Integrative analysis of anoikis-related prognostic signature to evaluate the immune landscape and predict therapeutic response in stomach adenocarcinoma.Scientific reports · 2025Article
- Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025Review
- Tripartite motif-containing protein 50 suppresses triple-negative breast cancer progression by regulating the epithelial-mesenchymal transition.Cancer biology & therapy · 2024Article
- HDAC10 switches NLRP3 modification from acetylation to ubiquitination and attenuates acute inflammatory diseases.Cell communication and signaling : CCS · 2024Article
- Chaperone-mediated autophagy modulates Snail protein stability: implications for breast cancer metastasis.Molecular cancer · 2024Article
- Emerging roles of tripartite motif family proteins (TRIMs) in breast cancer.Cancer medicine · 2024Review
- TRIM5 as a promising diagnostic biomarker of hepatocellular carcinoma: integrated analysis and experimental validation.Functional & integrative genomics · 2024Article
- TRIM22 induces cellular senescence by targeting PHLPP2 in hepatocellular carcinoma.Cell death & disease · 2024Article
- TRIM69 suppressed the anoikis resistance and metastasis of gastric cancer through ubiquitin‒proteasome-mediated degradation of PRKCD.Oncogene · 2023Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- TRIM50 Inhibits Gastric Cancer Progression by Regulating the Ubiquitination and Nuclear Translocation of JUP.Molecular cancer research : MCR · 2023Article
- USP2 promotes cell proliferation and metastasis in choroidal melanoma via stabilizing Snail.Journal of cancer research and clinical oncology · 2023Article
- The role of TRIM family in metabolic associated fatty liver disease.Frontiers in endocrinology · 2023Review
- TRIM50 promotes NLRP3 inflammasome activation by directly inducing NLRP3 oligomerization.EMBO reports · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif-containing 50 (TRIM50) belongs to the tripartite motif (TRIM) protein family, which has been implicated in the pathogenesis of multiple cancers. However, the role of TRIM50 in hepatocellular carcinoma (HCC) remains to be clarified. Here we showed that TRIM50 expression was significantly decreased in liver cancer tissues compared with corresponding non-cancerous liver tissues, and its decreased expression was significantly correlated with advanced disease progression. Gain-of-function assay by exogenous overexpression of TRIM50 in HCC cells showed that proliferation, colony formation, migration and invasion of HCC cells were significantly inhibited, whereas loss-of-function assay by TRIM50 knockdown showed that these malignant behaviors of HCC cells were significantly increased. Further investigation showed that TRIM50 could directly bind with SNAIL and induced K-48 linked poly-ubiquitous degradation of SNAIL protein, which further reversed SNAIL-mediated epithelial-to-mesenchymal transition (EMT) process of HCC cells. In vivo assay by xenograft tumor model verified the antitumor effect of TRIM50 on HCC. Taken together, these results showed that TRIM50 acted as a tumor suppressor in HCC cells by directly targeting SNAIL and reversing EMT, which further indicated that positive modulation of TRIM50 might be a novel therapeutic strategy for SNAIL overexpressed HCC cells.
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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.