ArticleJournal of cellular and molecular medicine2025
ZNF468/AURKA/PI3K/AKT Positive Feedback Loop Promotes Proliferation and Metastasis of Oesophageal Squamous Cell Carcinoma.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- ZNF468 stabilization by RNF4 enhances apoptosis resistance and carboplatin resistance in breast cancer via transcription activation of XIAP.Genes & genomics · 2026Article
- ZNF468/AURKA/PI3K/AKT Positive Feedback Loop Promotes Proliferation and Metastasis of Oesophageal Squamous Cell Carcinoma.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
While prior research linked ZNF468 to radioresistance in oesophageal squamous cell carcinoma (ESCC), its broader role in ESCC progression remained unclear. This study elucidates these functions and underlying mechanisms. Immunohistochemistry on clinical ESCC tissues demonstrated ZNF468 upregulation, which correlated with unfavourable patient outcomes and increased Aurora A expression. In vitro experiments, including assessments of proliferation, apoptosis, migration and invasion, revealed that ZNF468 overexpression enhanced these oncogenic phenotypes in ESCC cells, while its knockdown produced inhibitory effects. These findings were corroborated in vivo using subcutaneous tumour and lung metastasis models. Mechanistically, ZNF468 was found to upregulate AURKA expression, subsequently activating the PI3K/AKT signalling pathway, thereby promoting cell proliferation and epithelial-mesenchymal transition (EMT). Importantly, pharmacological inhibition of AURKA or the PI3K/AKT pathway significantly attenuated the pro-tumorigenic effects driven by ZNF468. Furthermore, AKT was shown to augment ZNF468 protein stability and transcriptional activity, establishing a ZNF468/AURKA/PI3K/AKT positive feedback loop. In conclusion, this study identifies a critical positive feedback mechanism involving ZNF468/AURKA/PI3K/AKT that significantly promotes ESCC progression, underscoring ZNF468 as a potential therapeutic target.
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.