ArticleMolecular and cellular pharmacology2009
Epigenetic Targeting of Transforming Growth Factor β Receptor II and Implications for Cancer Therapy.
Article in Molecular and cellular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 29 citations in OpenAlex.
- HC-HA/PTX3 from amniotic membrane reprograms human corneal fibroblasts to neural crest progenitors by switching from canonical to noncanonical TGFβ signaling.Stem cell research & therapy · 2026Article
- TGFβ signaling systems are prone to inhibition and ligand competition by coreceptor.bioRxiv : the preprint server for biology · 2026Article
- SYTL5 drives malignant progression in differentiated thyroid carcinoma: unveiling its regulatory mechanisms.Frontiers in oncology · 2026Article
- Exploring TGF-β Signaling in Cancer Progression: Prospects and Therapeutic Strategies.OncoTargets and therapy · 2025Review
- Curcumin Inhibition of TGFβ signaling in bone metastatic breast cancer cells and the possible role of oxidative metabolites.The Journal of nutritional biochemistry · 2022Article
- Review
- Identification and analysis of survival-associated ceRNA triplets in prostate adenocarcinoma.Oncology letters · 2019Article
- Review
- Axl is required for TGF-β2-induced dormancy of prostate cancer cells in the bone marrow.Scientific reports · 2016Article
- Inhibition of S-Adenosylmethionine-Dependent Methyltransferase Attenuates TGFβ1-Induced EMT and Metastasis in Pancreatic Cancer: Putative Roles of miR-663a and miR-4787-5p.Molecular cancer research : MCR · 2016Article
- Epigenetic: A missing paradigm in cellular and molecular pathways of sulfur mustard lung: a prospective and comparative study.Iranian journal of basic medical sciences · 2015Review
- TR4 nuclear receptor increases prostate cancer invasion via decreasing the miR-373-3p expression to alter TGFβR2/p-Smad3 signals.Oncotarget · 2015Article
- EZH2 promotes progression of small cell lung cancer by suppressing the TGF-β-Smad-ASCL1 pathway.Cell discovery · 2015Article
- Increased pSmad2 expression and cytoplasmic predominant presence of TGF-βRII in breast cancer tissue are associated with poor prognosis: results from the Shanghai Breast Cancer Study.Breast cancer research and treatment · 2015Article
- Clinical Implications of TβRII Expression in Breast Cancer.PloS one · 2015Article
- Article
- TGFβR2 is a major target of miR-93 in nasopharyngeal carcinoma aggressiveness.Molecular cancer · 2014Article
- Cell survival and metastasis regulation by Akt signaling in colorectal cancer.Cellular signalling · 2013Review
- Establishment and Validation of an Orthotopic Metastatic Mouse Model of Colorectal Cancer.ISRN hepatology · 2013Article
- Transforming growth factor-β in the gastrointestinal and hepatic tumor microenvironment.Gastroenterology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The transforming growth factor (TGF) β signaling pathway is involved in many cellular processes including proliferation, differentiation, adhesion, motility and apoptosis. The loss of TGFβ signaling occurs early in carcinogenesis and its loss contributes to tumor progression. The loss of TGFβ responsiveness frequently occurs at the level of the TGFβ type II receptor (TGFβRII) which has been identified as a tumor suppressor gene (TSG). In keeping with its TSG role, the loss of TGFβRII expression is frequently associated with high tumor grade and poor patient prognosis. Reintroduction of TGFβRII into tumor cell lines results in growth suppression. Mutational loss of TGFβRII has been characterized, particularly in a subset of colon cancers with DNA repair enzyme defects. However, the most frequent cause of TGFβRII silencing is through epigenetic mechanisms. Therefore, re-expression of TGFβRII by use of epigenetic therapies represents a potential therapeutic approach to utilizing the growth suppressive effects of the TGFβ signaling pathway. However, the restoration of TGFβ signaling in cancer treatment is challenging because in late stage disease, TGFβ is a pro-metastatic factor. This effect is associated with increased expression of the TGFβ ligand. In this Review, we discuss the mechanisms associated with TGFβRII silencing in cancer and the potential usefulness of histone deacetylase (HDAC) inhibitors in reversing this effect. The use of HDAC inhibitors may provide a unique opportunity to restore TGFβRII expression in tumors as their pleiotropic effects antagonize many of the cellular processes, which mediate the pro-metastatic effects associated with increased TGFβ expression.
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.