ArticleCancer research2015
ATDC/TRIM29 Drives Invasive Bladder Cancer Formation through miRNA-Mediated and Epigenetic Mechanisms.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 70 citations in OpenAlex.
- FGFR3-driven gene regulatory network analysis reveals a protumoral role for p63 in luminal bladder tumors.The Journal of clinical investigation · 2026Article
- TRIM29 is Critical for Bladder Cancer Progression and Modulates the Tumor-Immune Niche.Research square · 2026Article
- TRIM29 suppresses malignant progression in lung squamous cell carcinoma by shaping an immunosuppressive tumor microenvironment.Scientific reports · 2026Article
- TRIM29 promotes bladder cancer invasion by regulating the intermediate filament network and focal adhesion.Oncogene · 2025Article
- Review
- Article
- TRIM29 upregulation contributes to chemoresistance in triple negative breast cancer via modulating S100P-β-catenin axis.Cell communication and signaling : CCS · 2025Article
- Epigenetic modifications in bladder cancer: crosstalk between DNA methylation and miRNAs.Frontiers in immunology · 2025Review
- DNMT3a promotes LUAD cell proliferation and metastasis by activating the HDAC7 signalling pathway.International journal of biological sciences · 2025Article
- TRIM-endous functional network of tripartite motif 29 (TRIM29) in cancer progression and beyond.Cancer metastasis reviews · 2024Review
- Function of microRNA‑124 in the pathogenesis of cancer (Review).International journal of oncology · 2024Review
- TRIM29 acts as a potential senescence suppressor with epigenetic activation in nasopharyngeal carcinoma.Cancer science · 2023Article
- TRIM29 hypermethylation drives esophageal cancer progression via suppression of ZNF750.Cell death discovery · 2023Article
- The WAVE2/miR-29/Integrin-β1 Oncogenic Signaling Axis Promotes Tumor Growth and Metastasis in Triple-negative Breast Cancer.Cancer research communications · 2023Article
- The microRNA Lifecycle in Health and Cancer.Cancers · 2022Review
- A genome-wide association study with tissue transcriptomics identifies genetic drivers for classic bladder exstrophy.Communications biology · 2022Article
- microRNA-Mediated Encoding and Decoding of Time-Dependent Signals in Tumorigenesis.Biomolecules · 2022Review
- Association of H-Type Hypertension with miR-21, miR-29, and miR-199 in Kazahks of Xinjiang, China.International journal of hypertension · 2022Article
- Article
- CircIL4R activates the PI3K/AKT signaling pathway via the miR-761/TRIM29/PHLPP1 axis and promotes proliferation and metastasis in colorectal cancer.Molecular cancer · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Bladder cancer is a common and deadly malignancy but its treatment has advanced little due to poor understanding of the factors and pathways that promote disease. ATDC/TRIM29 is a highly expressed gene in several lethal tumor types, including bladder tumors, but its role as a pathogenic driver has not been established. Here we show that overexpression of ATDC in vivo is sufficient to drive both noninvasive and invasive bladder carcinoma development in transgenic mice. ATDC-driven bladder tumors were indistinguishable from human bladder cancers, which displayed similar gene expression signatures. Clinically, ATDC was highly expressed in bladder tumors in a manner associated with invasive growth behaviors. Mechanistically, ATDC exerted its oncogenic effects by suppressing miR-29 and subsequent upregulation of DNMT3A, leading to DNA methylation and silencing of the tumor suppressor PTEN. Taken together, our findings established a role for ATDC as a robust pathogenic driver of bladder cancer development, identified downstream effector pathways, and implicated ATDC as a candidate biomarker and therapeutic target.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.