ArticleAmerican journal of translational research2016
AKAP4 mediated tumor malignancy in esophageal cancer.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed, 13 citations in OpenAlex.
- Selection of tumor invasion-related genes to build a prognostic model and predict immune response and potential drugs for esophageal cancer patients based on WGCNA.Discover oncology · 2025Article
- High AKAP8L expression predicts poor prognosis in esophageal squamous cell carcinoma.Cancer cell international · 2022Article
- MiR-629-5p Promotes Prostate Cancer Development and Metastasis by Targeting AKAP13.Frontiers in oncology · 2021Article
- Role of A-Kinase anchor protein (AKAP4) in growth and survival of ovarian cancer cells.Oncotarget · 2017Article
- Silencing of A-Kinase Anchor Protein 4 (AKAP4) Inhibits Proliferation and Progression of Thyroid Cancer.Oncology research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AKAP4 as a new Cancer/Testis (CT) antigen is expressed not only in human germ cells, but also expressed in various tumor cells. AKAP4 is correlated with tumor malignancy; however, the role of AKAP4 in esophageal cancer remains unknown. Here we explored the function of AKAP4 in esophageal cancer. We found that AKAP4 mRNA and protein levels were up-regulated in the esophageal cancer tissues compared to normal control. In KYSE150 cell line, inhibition of AKAP4 suppressed cell growth and invasiveness. Overexpression of AKAP4 promoted cell growth and invasiveness. In addition, expression of epithelial markers (E-cadherin and ZO-1) was up-regulated or down-regulated and expression of mesenchymal markers (vimentin and N-cadherin) was down-regulated or up-regulated after knockdown or overexpression of AKAP4 in vitro. In vivo in a xenograft model silencing AKAP4 suppressed tumor growth. We also found that NF-κB p65 bound to AKAP4 promoter and regulated expression of AKAP4. In conclusion, overexpression of AKAP4 is associated with esophageal cancer progression. Inhibition of AKAP4 leads to suppressed growth and invasion of esophageal cancer.
Indexed as
Identifiers
27158351PMC4846908W2397316851What 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.