ReviewJournal of molecular medicine (Berlin, Germany)2021
Roles of E3 ubiquitin ligases in gastric cancer carcinogenesis and their effects on cisplatin resistance.
Review in Journal of molecular medicine (Berlin, Germany), 2021. 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 18 papers.
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Who cites it
18 citing papers in PubMed.
- FBXL5 depletion as a novel strategy against osteosarcoma: Evidence for MEK/ERK inhibition and enhanced therapeutic sensitivity.Oncology letters · 2026Article
- Targeting E3 ubiquitin ligases: Mechanistic breakthroughs and novel clinical translation pathways for tumor radioimmunotherapy.Molecular cancer · 2026Review
- In silico analysis of gene expression signatures and drug repurposing associated with metastatic progression in melanoma (skin cancer).Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The E3 ubiquitin ligase RNF180 modulates the EGFR/PI3K/AKT pathway to reduce cisplatin resistance in non-small cell lung cancer.Scientific reports · 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
- E3 ubiquitin ligases orchestrate chemo-resistance in gastrointestinal malignancies: from DNA damage response to therapeutic targeting.Frontiers in oncology · 2026Review
- Ginsenoside RG3 Synergizes With STING Agonist to Reverse Cisplatin Resistance in Gastric Cancer.Food science & nutrition · 2025Article
- Analysis of cullin family genes in rectal adenocarcinoma: expression, prognostic significance, and therapeutic implications.American journal of translational research · 2025Article
- RNF180 weakened the lipid droplet formation and subsequent chemoresistance by destabilizing ACC1 and ACLY in esophageal cancer.Frontiers in pharmacology · 2025Article
- Crosstalk among Alternative Polyadenylation, Genetic Variants and Ubiquitin Modification Contribute to Lung Adenocarcinoma Risk.International journal of molecular sciences · 2024Article
- Wnt signaling in gastric cancer: current progress and future prospects.Frontiers in oncology · 2024Review
- Mechanism of cisplatin resistance in gastric cancer and associated microRNAs.Cancer chemotherapy and pharmacology · 2023Review
- Methylomics and cancer: the current state of methylation profiling and marker development for clinical care.Cancer cell international · 2023Review
- Integrative analysis illustrates the role of PCDH7 in lung cancer development, cisplatin resistance, and immunotherapy resistance: an underlying target.Frontiers in pharmacology · 2023Article
- FBXW7 attenuates tumor drug resistance and enhances the efficacy of immunotherapy.Frontiers in oncology · 2023Review
- E3 ubiquitin ligases and deubiquitinases in bladder cancer tumorigenesis and implications for immunotherapies.Frontiers in immunology · 2023Review
- Droplet digital polymerase chain reaction assay for methylated ring finger protein 180 in gastric cancer.World journal of gastrointestinal oncology · 2022Article
- Glaucocalyxin A Inhibits the Malignancies of Gastric Cancer Cells by Downregulating MDM2 and RNF6Frontiers in oncology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although gastric cancer (GC) is one of the most common cancers with high incidence and mortality rates, its pathogenesis is still not elucidated. GC carcinogenesis is complicated and involved in the activation of oncoproteins and inactivation of tumor suppressors. The ubiquitin-proteasome system (UPS) is crucial for protein degradation and regulation of physiological and pathological processes. E3 ubiquitin ligases are pivotal enzymes in UPS, containing various subfamily proteins. Previous studies report that some E3 ligases, including SKP2, CUL1, and MDM2, act as oncoproteins in GC carcinogenesis. On the other hand, FBXW7, FBXL5, FBXO31, RNF43, and RNF180 exert as tumor suppressors in GC carcinogenesis. Moreover, E3 ligases modulate cell growth, cell apoptosis, and cell cycle; thus, it is complicated to confer cisplatin resistance/sensitivity in GC cells. The intrinsic and acquired cisplatin resistance limits its clinical application against GC. In this review, we explore oncogenic and tumor suppressive roles of E3 ligases in GC carcinogenesis and focus on the effects of E3 ligases on cisplatin resistance in GC cells, which will provide novel therapeutic targets for GC therapy, especially for cisplatin-resistant 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.