ArticleJournal of translational medicine2024
CPSF4-mediated regulation of alternative splicing of HMG20B facilitates the progression of triple-negative breast cancer.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Knockdown of STK39 inhibits lung cancer brain metastasis by suppressing the CPSF4/NFκB/COX2 pathway.Journal of neuro-oncology · 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAberrant alternative splicing (AS) contributes to tumor progression. A crucial component of AS is cleavage and polyadenylation specificity factor 4 (CPSF4). It remains unclear whether CPSF4 plays a role in triple-negative breast cancer (TNBC) progression through AS regulation. In this study, our objective is to investigate the prognostic value of CPSF4 and pinpoint pivotal AS events governed by CPSF4 specifically in TNBC.
methodsWe examined the expression levels and prognostic implications of CPSF4 in patients diagnosed with TNBC through public databases. CPSF4-interacting transcripts, global transcriptome, and alternative splicing were captured through RNA immunoprecipitation sequencing (RIP-seq) and RNA sequencing (RNA-seq). The top 10 CPSF4-regulated alternative splicing events (ASEs) were validated using qRT-PCR. TNBC cells transfected with high mobility group 20B (HMG20B) siRNA were subjected to CCK-8 and transwell assays.
resultsIn TNBC, CPSF4 exhibited heightened expression levels and was correlated with unfavorable prognosis. Overexpression of CPSF4 significantly promoted colony formation and migration, whereas knockdown of CPSF4 had the opposite effect. Inhibition of CPSF4 altered the transcriptome profile of MDA-MB-231 cells. CPSF4-regulated numerous genes showed enrichment in cancer-related functional pathways, including mRNA processing, cell cycle, RNA transport, mRNA surveillance pathway, and apoptosis. CPSF4-regulated ASEs were highly validated by qRT-PCR. CPSF4 modulated selective splicing events by inhibiting alternative 3' splice site events of HMG20B and promoted cell proliferation, migration, and invasion.
conclusionCPSF4 promotes TNBC progression by regulating AS of HMG20B. These findings contribute to the development of more useful prognostic, diagnostic and potentially therapeutic biomarkers for TNBC.
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.