ArticleJournal of oncology2022
Upregulated Circular RNA KIF4A Promotes Cell Migration and Invasion by Regulating MicroRNA-144-3p/EZH2 Axis in Gastric Cancer.
Article in Journal of oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- From inflammation to carcinogenesis: MiRNA regulates epithelial-mesenchymal transition to facilitate malignant progression of gastric precancerous lesions.Frontiers in oncology · 2026Review
- KIF4A in disease pathogenesis and therapeutics: from molecular mechanisms to clinical translation.Biology direct · 2025Review
- Review
- Review
- ENTPD1-AS1-miR-144-3p-mediated high expression ofWorld journal of gastrointestinal oncology · 2023Article
- CircKIF4A promotes glioma growth and temozolomide resistance by accelerating glycolysis.Cell death & disease · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence has shown that circular RNAs (circRNAs) serve a critical regulatory role in various human cancers, including gastric cancer (GC), and in this study, we aimed to explore the functions of circKIF4A in the progression of GC. Our findings demonstrated that circKIF4A was highly expressed in both GC tissues and cell lines, and high intratumoral circKIF4A expression predicted a poor prognosis in GC patients. In vitro gain- and loss-of-function assays indicated that circKIF4A knockdown suppressed the proliferation, migration, invasion, and EMT of GC cells, while these malignant behaviors were enhanced by circKIF4A overexpression. Mechanistically, we found that circKIF4A was mainly located in the cytoplasm, could directly interact with microRNA- (miR-) 144-3p, and functions as a miRNA sponge to regulate EZH2 expression in GC cells. miR-144-3p inhibition or EZH2 restoration largely blocked the effects of circKIF4A knockdown on the malignant behaviors of GC cells. This study indicated that circKIF4A can efficiently sponge miR-144-3p to promote the malignant behaviors of GC cells and may provide a potential biomarker and therapeutic target for GC management.
Identifiers
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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.