ReviewInternational journal of molecular sciences2013
The dual role of Smad7 in the control of cancer growth and metastasis.
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- Pooled it
- SMAD7-Associated Glycolytic Regulation Promotes Lactate-Dependent Macrophage Phenotype Modulation in Colorectal Cancer.Cancers · 2026Article
- HDAC2-Mediated SMAD7 Stabilisation Activates Wnt/β-Catenin Signalling to Drive DNA Damage Repair and Cisplatin Resistance in Ovarian Cancer.Journal of cellular and molecular medicine · 2026Article
- Elongationless start-stop elements are stress-resilient translation gates that are more repressive than uTranslons.Nucleic acids research · 2026Article
- The YTHDC1/HECW1/SMAD7 axis drives cisplatin resistance in bladder cancer.Translational andrology and urology · 2026Article
- Review
- Murine toxicology assessment of avgn7.2, a novel gene therapeutic for inclusion body myositis and other muscle wasting diseases.Gene therapy · 2026Article
- Codon-optimized human Smad7 gene therapy enhances skeletal muscle mass and function in a murine model of Duchenne muscular dystrophy.Gene therapy · 2026Article
- Smad7 is a negative regulator of immunogenic cell death in colorectal cancer.Oncoimmunology · 2025Article
- Advancing Colorectal Cancer Diagnostics from Barium Enema to AI-Assisted Colonoscopy.Diagnostics (Basel, Switzerland) · 2025Review
- Uncovering immune cell heterogeneity in hepatocellular carcinoma by combining single-cell RNA sequencing with T-cell receptor sequencing.World journal of hepatology · 2025Article
- KAT2B inhibits proliferation and invasion via inactivating TGF-β/Smad3 pathway-medicated autophagy and EMT in epithelial ovarian cancer.Scientific reports · 2025Article
- miRNAs in Signal Transduction of SMAD Proteins in Breast Cancer.International journal of molecular sciences · 2024Article
- Theranostic imaging and multimodal photodynamic therapy and immunotherapy using the mTOR signaling pathway.Nature communications · 2023Article
- Long non-coding RNAs as the critical regulators of PI3K/AKT, TGF-β, and MAPK signaling pathways during breast tumor progression.Journal of translational medicine · 2023Review
- ALKBH1-mediated mMolecular oncology · 2023Article
- Article
- Regulation of transforming growth factor-β signaling as a therapeutic approach to treating colorectal cancer.World journal of gastroenterology · 2022Review
- MiR-410-3p facilitates Angiotensin II-induced cardiac hypertrophy by targeting Smad7.Bioengineered · 2022Article
- Expression and function of Smad7 in autoimmune and inflammatory diseases.Journal of molecular medicine (Berlin, Germany) · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smad7 was initially identified as an inhibitor of Transforming growth factor (TGF)-β due mainly to its ability to bind TGF-β receptor type I and prevent TGF-β-associated Smad signaling. More recently, it has been demonstrated that Smad7 can interact with other intracellular proteins and regulate also TGF-β-independent signaling pathways thus making a valid contribution to the neoplastic processes in various organs. In particular, data emerging from experimental studies indicate that Smad7 may differently modulate the course of various tumors depending on the context analyzed. These observations, together with the demonstration that Smad7 expression is deregulated in many cancers, suggest that therapeutic interventions around Smad7 can help interfere with the development/progression of human cancers. In this article we review and discuss the available data supporting the role of Smad7 in the modulation of cancer growth and progression.
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.