ArticleThe American journal of pathology2012
TRIM29 functions as a tumor suppressor in nontumorigenic breast cells and invasive ER+ breast cancer.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 2026Review
- TRIM29 suppresses malignant progression in lung squamous cell carcinoma by shaping an immunosuppressive tumor microenvironment.Scientific reports · 2026Article
- TRIM29 upregulation contributes to chemoresistance in triple negative breast cancer via modulating S100P-β-catenin axis.Cell communication and signaling : CCS · 2025Article
- TRIM-endous functional network of tripartite motif 29 (TRIM29) in cancer progression and beyond.Cancer metastasis reviews · 2024Review
- TRIM25, TRIM28 and TRIM59 and Their Protein Partners in Cancer Signaling Crosstalk: Potential Novel Therapeutic Targets for Cancer.Current issues in molecular biology · 2024Review
- High expression of the RET receptor tyrosine kinase and its ligand GDNF identifies a high-risk subset of estrogen receptor positive breast cancer.Breast cancer research and treatment · 2023Article
- A genome-wide association study with tissue transcriptomics identifies genetic drivers for classic bladder exstrophy.Communications biology · 2022Article
- TRIM family contribute to tumorigenesis, cancer development, and drug resistance.Experimental hematology & oncology · 2022Review
- TRIM29 in Cutaneous Squamous Cell Carcinoma.Frontiers in medicine · 2021Review
- TRIM29 Reverses Oxaliplatin Resistance of P53 Mutant Colon Cancer Cell.Canadian journal of gastroenterology & hepatology · 2021Article
- Loss of TRIM29 suppresses cancer stem cell-like characteristics of PDACs via accelerating ISG15 degradation.Oncogene · 2020Article
- Overexpression of sigma-1 receptor in MCF-7 cells enhances proliferation via the classic protein kinase C subtype signaling pathway.Oncology letters · 2018Article
- MicroRNA‑122 acts as tumor suppressor by targeting TRIM29 and blocking the activity of PI3K/AKT signaling in nasopharyngeal carcinoma in vitro.Molecular medicine reports · 2018Article
- Epigenetic landscape change analysis during human EMT sheds light on a key EMT mediator TRIM29.Oncotarget · 2017Article
- Bioinformatics analysis of the prognostic value of Tripartite Motif 28 in breast cancer.Oncology letters · 2017Article
- microRNA-761 induces aggressive phenotypes in triple-negative breast cancer cells by repressing TRIM29 expression.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- The Breast Cancer Tumor Suppressor TRIM29 Is Expressed via ATM-dependent Signaling in Response to Hypoxia.The Journal of biological chemistry · 2016Article
- TRIM29 Overexpression Promotes Proliferation and Survival of Bladder Cancer Cells through NF-κB Signaling.Cancer research and treatment · 2016Article
- TRIM29 overexpression is associated with poor prognosis and promotes tumor progression by activating Wnt/β-catenin pathway in cervical cancer.Oncotarget · 2016Article
- Grainyhead-like 2 downstream targets act to suppress epithelial-to-mesenchymal transition during neural tube closure.Development (Cambridge, England) · 2016Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Tripartite motif-containing 29 (TRIM29) is a member of the TRIM protein family that has been implicated in hematologic and solid tumor cancers. We found that TRIM29 functions as a tumor suppressor in both the nontumorigenic MCF10A [estrogen receptor (ER)-/TRIM29+] breast cell line and the invasive MCF7 (ER+/TRIM29-) breast cell line. Silencing TRIM29 in MCF10A cells resulted in preneoplastic changes that included loss of polarity in three-dimensional culture, increased proliferation, anchorage-independent growth, and increased migration and invasion. Conversely, the introduction of TRIM29 into MCF7 cells caused reversion to a less aggressive phenotype by antagonizing the growth effect of 17β-estradiol. The interaction between TRIM29 and ER signaling in MCF7 cells was supported by a reduction in ERE binding in the presence of TRIM29 and suppression of ER-dependent gene expression of TFF1, FOS, and GREB1. By microarray analyses, we showed that younger women (<55 years of age) with early-stage, ER+ breast cancer who were given no adjuvant systemic therapy had a significantly lower risk of relapse when their tumor had high TRIM29 expression (P = 0.02). This effect was not observed in older women (>55 years of age) and thus may be due to menopause and loss of circulating estrogens. Our results suggest that loss of TRIM29 expression in normal breast luminal cells can contribute to malignant transformation and lead to progression of ER+ breast cancer in premenopausal women.
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