ArticleGastroenterology2007
Activin type 2 receptor restoration in MSI-H colon cancer suppresses growth and enhances migration with activin.
Article in Gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 60 citations in OpenAlex.
- Bone morphogenetic proteins, activins, and growth and differentiation factors in tumor immunology and immunotherapy resistance.Frontiers in immunology · 2022Review
- An inflammatory response-related gene signature associated with immune status and prognosis of acute myeloid leukemia.American journal of translational research · 2022Article
- AT Homopolymer Strings inMicroorganisms · 2021Article
- Dual Roles of the Activin Signaling Pathway in Pancreatic Cancer.Biomedicines · 2021Review
- Profiling Activins and Follistatin in Colorectal Cancer According to Clinical Stage, Tumour Sidedness and Smad4 Status.Pathology oncology research : POR · 2021Article
- Discovery and Structure-Activity Relationship Study of (Journal of medicinal chemistry · 2020Article
- Microsatellite Instability-RelatedOncoTargets and therapy · 2020Article
- Exome-wide somatic mutation characterization of small bowel adenocarcinoma.PLoS genetics · 2018Article
- Activin in acute pancreatitis: Potential risk-stratifying marker and novel therapeutic target.Scientific reports · 2017Article
- Activin signaling is an essential component of the TGF-β induced pro-metastatic phenotype in colorectal cancer.Scientific reports · 2017Article
- NFkB is essential for activin-induced colorectal cancer migration via upregulation of PI3K-MDM2 pathway.Oncotarget · 2017Article
- Article
- Microsatellite Instability Pathway and EMAST in Colorectal Cancer.Current colorectal cancer reports · 2017Article
- Activins and their related proteins in colon carcinogenesis: insights from early and advanced azoxymethane rat models of colon cancer.BMC cancer · 2016Article
- GRG Profiles: John M. Carethers.Digestive diseases and sciences · 2016Article
- Commentary: Activin and TGFβ use diverging mitogenic signaling in advanced colon cancer.Journal of rare diseases research & treatment · 2016Article
- Activin and TGFβ use diverging mitogenic signaling in advanced colon cancer.Molecular cancer · 2015Article
- Genetics and Genetic Biomarkers in Sporadic Colorectal Cancer.Gastroenterology · 2015Review
- Malignant pleural mesothelioma: history, controversy and future of a manmade epidemic.European respiratory review : an official journal of the European Respiratory Society · 2015Review
- De Novo proteome analysis of genetically modified tumor cells by a metabolic labeling/azide-alkyne cycloaddition approach.Molecular & cellular proteomics : MCP · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND &
aimsColon cancers with high-frequency microsatellite instability (MSI-H) develop frameshift mutations in tumor suppressors as part of their pathogenesis. ACVR2 is mutated at its exon 10 polyadenine tract in >80% of MSI-H colon cancers, coinciding with loss of protein. ACVR2 transmits the growth effects of activin via phosphorylation of SMAD proteins to affect gene transcription. The functional effect of activin in colon cancers has not been studied. We developed and characterized a cell model in which we studied how activin signaling affects growth.
methodshMLH1 and ACVR2 mutant HCT116 cells were previously stably transferred with chromosome 2 (HCT116+chr2), restoring a single regulated copy of wild-type ACVR2 but not hMLH1. Both HCT116+chr2 and parental HCT116 cells (as well as HEC59 and ACVR2 and hMSH2 complemented HEC59+chr2 cells) were assessed for genetic complementation and biologic function.
resultsHCT116+chr2 cells and HEC59+chr2 cells, but not ACVR2-mutant HCT116 or HEC59 cells, acquired wild-type ACVR2 as well as expression of ACVR2 wild-type messenger RNA. Complemented ACVR2 protein complexed with ACVR1 with activin treatment, generating nuclear phosphoSMAD2 and activin-specific gene transcription. ACVR2-restored cells showed decreased growth and reduced S phase but increased cellular migration following activin treatment. ACVR2 small interfering RNA reversed these effects in complemented cells.
conclusionsACVR2-complemented MSI-H colon cancers restore activin-SMAD signaling, decrease growth, and slow their cell cycle following ligand stimulation but show increased cellular migration. Activin is growth suppressive and enhances migration similar to transforming growth factor beta in colon cancer, indicating that abrogation of the effects of activin contribute to the pathogenesis of MSI-H colon cancers.
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.