ArticleCancer cell international2020
TRIM3 inhibits P53 signaling in breast cancer cells.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 39 citations in OpenAlex.
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 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
- TRIM3 exacerbates chondrocyte apoptosis through suppression of AKT/mTOR signaling pathway in osteoarthritis.Journal of orthopaedic surgery and research · 2025Article
- The Molecular Mechanism ofInternational journal of molecular sciences · 2025Article
- An investigation of the molecular characterization of the tripartite motif (TRIM) family and primary validation of TRIM31 in gastric cancer.Human genomics · 2024Article
- Emerging roles of tripartite motif family proteins (TRIMs) in breast cancer.Cancer medicine · 2024Review
- Advances in the antitumor mechanisms of tripartite motif-containing protein 3.Journal of cancer research and clinical oncology · 2024Review
- Telomerase and mitochondria inhibition promote apoptosis and TET2 and ANMT3a expression in triple negative breast cancer cell lines.BioImpacts : BI · 2024Article
- TRIM3 facilitates ferroptosis in non-small cell lung cancer through promoting SLC7A11/xCT K11-linked ubiquitination and degradation.Cell death and differentiation · 2024Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- TRIM3 and TRIM16 as potential tumor suppressors in breast cancer patients.BMC research notes · 2022Article
- TRIM3 facilitates estrogen signaling and modulates breast cancer cell progression.Cell communication and signaling : CCS · 2022Article
- Tripartite Motif Containing 3 inhibits the aggressive behaviors of papillary thyroid carcinoma and indicates lower recurrence risk.Genes & genomics · 2022Article
- Decreased expression of TRIM3 gene predicts a poor prognosis in gastric cancer.Journal of gastrointestinal cancer · 2022Article
- Comprehensive Analysis of the Expression and Prognosis for Tripartite Motif-Containing Genes in Breast Cancer.Frontiers in genetics · 2022Article
- Knockdown of Brachyury Suppresses Breast Cancer Cell Proliferation and Migration via Targeting E2F3.Journal of oncology · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBeast cancer is the most common women cancer worldwide, while two third of them are ER alpha positive breast cancer. Among the ER alpha positive breast cancer, about 80% are P53 wild type, indicating the potential tumor suppression role in ER alpha positive breast cancer. Since P53 is an important safeguard to inhibit cell malignant transformation, reactivating P53 signaling could a plausible approach to treat breast cancer.
methodsTRIM3 protein levels were measured by western blot, while the P53 classical target genes were measured by real-time PCR. WST1 assay were used to measure cell proliferation, while cleaved caspase-3 was used to detect cell apoptosis. Protein stability and ubiquitin assay were used to detect the P53 protein ubiquitin and stability. The immuno-precipitation assays were used to detect the protein interactions. Immuno-staining was used to detect the protein localization of P53 and TRIM3, while the ubiquitin-based immuno-precipitation assays were used to detect the specific ubiquitination manner of P53.
resultsIn our study, we identified TRIM3 as an endogenous inhibitor for P53 signaling. TRIM3 depletion inhibited breast cancer cell proliferation and promoted apoptosis. In addition, TRIM3 depletion increased P53 protein level in breast cancer cell. Further investigation showed that TRIM3 could associate with P53 and promote P53 K48-linked ubiquitination and degradation.
conclusionOur study identified a novel post-translational modification mechanism between TRIM3 and P53. TRIM3 depletion or blockage could be a promising strategy to rescue P53 signaling and inhibit breast cancer progression.
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