ArticleGenes & genomics2026
ZNF468 stabilization by RNF4 enhances apoptosis resistance and carboplatin resistance in breast cancer via transcription activation of XIAP.
Article in Genes & genomics, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCarboplatin is a commonly utilized chemotherapy agent for breast cancer treatment, yet resistance to this drug remains a significant clinical challenge
objectiveThe objective of this study was to investigate the role and regulatory mechanism of zinc finger protein 468 (ZNF468) in carboplatin resistance in breast cancer.
methodsTo establish carboplatin-resistant cells, SK-BR-3 and MDA-MB-231 cells were exposed to increasing concentrations of carboplatin. ZNF468 expression was analyzed in clinical samples (carboplatin-resistant vs. sensitive patients, n=40) and carboplatin-resistant cells. Functional assays, including Cell Counting Kit-8 (CCK-8), EDU staining, flow cytometry, and colony formation assays, were conducted to evaluate cell viability and apoptosis. The interactions and underlying mechanisms were further explored using Chromatin immunoprecipitation (ChIP), luciferase reporter assays, co-immunoprecipitation (Co-IP), and cycloheximide chase assays.
resultsZNF468 was significantly elevated in carboplatin-resistant cells and tissues. Knockdown of ZNF468 reduced the growth of cells and increased apoptosis in drug-resistant cells. ZNF468 was found to transcriptionally activate X-linked inhibitor of apoptosis protein (XIAP), which contributed to enhanced resistance to apoptosis and carboplatin. In addition, RING Finger Protein 4 (RNF4) was shown to stabilize ZNF468 by promoting its phosphorylation, and this stabilization further aggravated the resistance to apoptosis and carboplatin treatment in breast cancer cells.
conclusionRNF4 stabilized ZNF468, which transcriptionally activates XIAP, enhancing resistance to apoptosis and promoting carboplatin resistance in breast cancer. This study highlights the critical role of ZNF468 in carboplatin resistance, providing potential therapeutic targets for overcoming drug resistance in breast cancer treatment.
Indexed as
Identifiers
42053881What 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.