ArticleInvestigational new drugs2021
The E3 ligase HUWE1 mediates TGFBR2 ubiquitination and promotes gastric cancer cell proliferation, migration, and invasion.
Article in Investigational new drugs, 2021. 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, 15 citations in OpenAlex.
- The multifaceted role of E3 ubiquitin ligases in cancer metastasis: mechanisms, targets, and therapeutic implications.Essays in biochemistry · 2025Review
- Construction and validation of a post-translational modification-related signature to predict the effect of immune therapies in gastric cancer.Biochemistry and biophysics reports · 2025Article
- Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025Review
- UPS: Opportunities and challenges for gastric cancer treatment.Frontiers in oncology · 2023Review
- Emerging roles of the HECT E3 ubiquitin ligases in gastric cancer.Pathology oncology research : POR · 2023Review
- CRISPR screening of E3 ubiquitin ligases reveals Ring Finger Protein 185 as a novel tumor suppressor in glioblastoma repressed by promoter hypermethylation and miR-587.Journal of translational medicine · 2022Article
- Identification of Hub Genes Associated With the Development of Stomach Adenocarcinoma by Integrated Bioinformatics Analysis.Frontiers in oncology · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HUWE1, as a well-known E3 ligase, has an oncogenic or tumor-suppressive role in various cancers by mediating ubiquitination and degradation of substrates. However, the role and action mechanism of HUWE1 in gastric cancer (GC) remain unclear. This study aimed to investigate whether HUWE1 plays a role in GC development in vitro by mediating transforming growth factor-β receptor 2 (TGFBR2) ubiquitination and degradation. HUWE1 was overexpressed in SGCA-7901 GC cells and silenced in MGC-803 GC cells. Then, GC cell proliferation, migration, and invasion were evaluated by MTT assay and Transwell migration and invasion assay, respectively. The regulatory effect and mechanism of HUWE1 on TGFBR2 expression were assessed by qRT-PCR, western blot, and ubiquitination assay. HUWE1 mRNA and protein levels were higher in human GC tissues than in matched noncancerous gastric tissues. HUWE1 overexpression promoted, whereas HUWE1 silencing inhibited GC cell proliferation, migration, and invasion. HUWE1 promoted ubiquitination and degradation of TGFBR2. TGFBR2 overexpression impaired the tumor-promoting effect of HUWE1 overexpression in regulating GC cell behaviors. HUWE1 promoted GC cell proliferation, migration, and invasion, at least partially, by mediating TGFBR2 ubiquitination. Our data indicated a novel regulatory mechanism of HUWE1 in GC development, and provided a potential idea for the disease treatment.
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