ArticleMolecular medicine reports2026
Zinc finger protein 514 promotes esophageal cancer progression by enhancing cell proliferation, migration and invasion.
Article in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal cancer (EC), a malignant tumor occurring in the upper gastrointestinal tract, is the seventh most common cancer worldwide. Zinc finger proteins (ZNFs), the most abundant family of transcription factors in humans, serve an important role in the initiation and progression of various malignant tumors. However, the function of ZNFs in EC remains unclear. The present study aimed to elucidate the role of ZNF514 in the development and progression of EC and to investigate its underlying mechanism. The mRNA and protein expression levels of ZNF514 were assessed using reverse transcription‑quantitative PCR and western blotting. To assess functional roles, multiple cellular assays were performed, including 5‑ethynyl‑2'‑deoxyuridine incorporation, Cell Counting Kit‑8, wound healing, colony formation and Transwell assays. Subsequently, for transcriptomics analysis, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses, Gene Set Enrichment Analysis and Ingenuity Pathway Analysis (IPA) were performed. In EC, ZNF514 exhibited high expression at both the mRNA and protein levels. Additionally, ZNF514 influenced the migration, invasion and proliferation of EC cells. Gene enrichment analyses and IPA demonstrated that ZNF514 knockdown significantly affected multiple signaling pathways, such as Fcγ receptors, the complement system, G‑protein coupled receptors (GPCRs)‑related receptors, the ribosomal S6 kinase (RSK) pathway, Ras/MEK, PI3K/AKT, STAT3, nucleotide‑binding oligomerization domain‑containing protein (NOD) and NF‑κB pathways. In conclusion, the present study indicated that the anticancer mechanisms induced by ZNF514 knockdown may be related to the enhancement of Fcγ receptor and complement system activation, as well as the inhibition of GPCR, RSK, Ras/MEK, PI3K/AKT, STAT3, NOD1/2 and NF‑κB pathways.
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.