ArticleCytotechnology2025
The regulatory role of KIAA1429 in epithelial-mesenchymal transition in cervical cancer via mediating m6A modification of BTG2.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Low-molecular-weight metabolites from lactic acid bacteria suppress cervical cancer progression by inhibiting EMT via the Wnt/β-catenin pathway.Open life sciences · 2026Article
- N6-methyladenosine in cervical carcinogenesis: Mechanistic insights and therapeutic perspectives (Review).Oncology letters · 2025Review
- The Multifaceted Role of VIRMA, a Core Component of the Methyltransferase Complex, in Cancer and Cancer Therapy.Biomolecules · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer (CC) represents one of the important cancers affecting global female population worldwide. We sought to elucidate the roles and mechanisms of KIAA1429 in the malignant properties of CC cells and the epithelial-mesenchymal transition (EMT) process. KIAA1429 was predicted to be abnormally expressed in CC and correlate with shortened survival of CC patients by GEPIA2 and GSCA databases. High expression of KIAA1429 in human CC cell lines (SiHa, HT-3) was validated by RT-qPCR and Western blot assays. A series of small interfering (si)RNAs including si-KIAA1429-1, si-KIAA1429-2, si-YTHDF2, si-BTG2, and si-negative control (NC) were utilized to interfere the expression levels of KIAA1429, YTHDF2, and BTG2, respectively. Consequently, KIAA1429 silencing attenuated the proliferation, migratory, and invasive functions of CC cells and repressed EMT while promoting CC cell apoptosis. Mechanistically, KIAA1429 could affect N6-methyladenosine (m6A) modification to attenuate the stability of BTG2 mRNA and down-regulate its expression. Additionally, loss of BTG2 partly counteracted the effects of si-KIAA1429 on repressing the malignant activities of CC cells. The aforementioned results collectively demonstrated that KIAA1429-mediated m6A modification of BTG2 and contributed to malignant progression of CC in vitro. Supplementary Information: The online version contains supplementary material available at 10.1007/s10616-024-00694-3.
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.