ArticleScientific reports2019
Activin A regulates the epidermal growth factor receptor promoter by activating the PI3K/SP1 pathway in oral squamous cell carcinoma cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 23 citations in OpenAlex.
- Activin A enhances neurofunctional recovery following traumatic spinal cord injury by inhibiting autophagy.Neural regeneration research · 2026Article
- Activin A-Targeted Therapy in Cancer: An Updated Review on Challenges and Opportunities in Clinical Translation.Current pharmaceutical design · 2026Review
- Activin A affects colorectal cancer progression and immunomodulation in a stage dependent manner.Scientific reports · 2025Article
- Dysregulated PI3K/AKT signaling in oral squamous cell carcinoma: The tumor microenvironment and epigenetic modifiers as key drivers.Oncology research · 2025Review
- Article
- Hepsin promotes breast tumor growth signaling via the TGFβ-EGFR axis.Molecular oncology · 2024Article
- Dihydromyrcenol Modulates Involucrin Expression through the Akt Signaling Pathway.International journal of molecular sciences · 2024Article
- Article
- Potential Roles of Activin in Head and Neck Squamous Cell Carcinoma Progression and Mortality.Anticancer research · 2023Article
- Identification of multidrug chemoresistant genes in head and neck squamous cell carcinoma cells.Molecular cancer · 2023Article
- Evolution of the ErbB gene family and analysis of regulators ofNeural regeneration research · 2022Article
- Role of PI3K/AKT pathway in squamous cell carcinoma with an especial focus on head and neck cancers.Cancer cell international · 2022Review
- Comprehensive analysis of INHBA: A biomarker for anti-TGFβ treatment in head and neck cancer.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway.Cell death discovery · 2022Article
- Percentage genome change and chromosome 7q amplification predict sorafenib response in advanced hepatocellular carcinoma.Biomedical journal · 2021Article
- Novel biomarkers for subtle myocardial involvement in type I diabetes mellitus.Cardiovascular endocrinology & metabolism · 2021Article
- Article
- Human Papillomavirus Infection in Head and Neck Squamous Cell Carcinomas: Transcriptional Triggers and Changed Disease Patterns.Frontiers in cellular and infection microbiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal growth factor receptor (EGFR) and activin A are both overexpressed in oral cavity squamous cell carcinoma (OSCC). We evaluated their clinical correlation and activin A-mediated EGFR regulation in this study. Overexpression of both transcripts/proteins indicated a poorer prognosis in OSCC patients. Knockdown of endogenous INHBA repressed the expression of EGFR and inhibited activin A-mediated canonical Smads, noncanonical phosphorylation of AKT (ser473) (p-AKT ser473) and SP1. Inhibition of PI3K signaling via its inhibitor attenuated p-AKT ser473 and in turn reduced SP1 and EGFR expression in the presence of recombinant activin A (rActivin A) in OSCC cells, as revealed via a luciferase assay and western blotting. However, canonical Smad signaling repressed the EGFR promoter, as revealed by a luciferase assay. The transcription factor SP1, its coactivator CBP/p300, and Smad proteins were recruited to the EGFR proximal promoter following rActivin A treatment, as revealed by chromatin immunoprecipitation (ChIP). Smad2/3/4 dramatically outcompeted SP1 binding to the EGFR proximal promoter following mithramycin A treatment. Activin A activates the PI3K and Smad pathways to compete for binding to overlapping SP1 consensus sequences on the EGFR proximal promoter. Nevertheless, canonical p-Smad2 was largely repressed in OSCC tumor tissues, suggesting that the activin A-mediated noncanonical pathway is essential for the carcinogenesis of OSCC.
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.