ArticleDiscover oncology2025
PARP14-mediated glycolysis enhances Tamoxifen resistance in estrogen receptor + breast cancer cells.
Article in Discover oncology, 2025. 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.
- Structure, function, regulation, evolution, and therapeutic implications of PARP14.Genes & development · 2026Review
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
Abstract
backgroundResistance to Tamoxifen is a major challenge in the therapeutic management of estrogen receptor (ER) + breast cancer (BC). Glycolysis, as reported, exerts a crucial influence on the regulation of Tamoxifen resistance in BC, highlighting the need for further investigation into the mechanisms by which it contributes to Tamoxifen resistance in ER + BC.
methodBioinformatics was employed to analyze the differential expression of PARP14 between Tamoxifen-responsive and -resistant ER + BC tissues. Poly (ADP-ribose) polymerase family member 14 (PARP14) expression in Tamoxifen-resistant cell lines (T47D/TAMR) was quantified through quantitative real time polymerase chain reaction (qRT-PCR). A subsequent Gene Set Enrichment Analysis (GSEA) was conducted to determine the relationship between PARP14 and glycolysis-related genes. The assessment of glycolytic activity included measurements of hexokinase II (HK2) expression, extracellular acidification rate (ECAR), oxygen consumption rate (OCR), glucose uptake, lactate secretion, and adenosine Triphosphate (ATP) synthesis. Cellular proliferation was evaluated using a colony formation assay, cell viability was assessed with the Cell Counting Kit-8 (CCK-8) assay to establish the half maximal inhibitory concentration (IC
resultsPARP14 exhibited elevated expression in Tamoxifen-resistant tissues and cells such as T47D/TAMR, where its knockdown increased responsiveness to Tamoxifen. PARP14 was also notably associated with the glycolysis pathway, showing a positive correlation with genes that enhance glycolysis, and its suppression led to decreased glycolysis in T47D/TAMR cells. Overexpression of PARP14 in vitro induced Tamoxifen resistance in these cells, but co-administration of the glycolytic inhibitor 2-DG could recover their sensitivity to Tamoxifen.
conclusionPARP14 facilitates Tamoxifen resistance in ER + BC cells via the activation of the glycolysis pathway. We suspect that targeting PARP14 or the glycolytic pathway could be a viable therapeutic option for ER + BC that has developed resistance to Tamoxifen.
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.