ArticleJournal of breast cancer2025
Loss of Nuclear Profilin 1 Triggers Oncogenic Reprogramming of Mammary Epithelial Cells Through Dysregulated DNA Replication in Breast Cancer.
Article in Journal of breast cancer, 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.
- Profilin-1 Deficiency Activates STING to Drive T Cell-Mediated Anti-Tumor Immunity in Breast Cancer.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
purposeProfilin 1 (Pfn1) has been implicated in cytoskeletal regulation; however, its role in breast cancer progression and DNA replication remains unclear. This study investigated the functional significance of Pfn1 nuclear-cytoplasmic shuttling in breast cancer.
methodsWe analyzed Pfn1 expression and its correlation with DNA replication, repair, and oncogenic markers in breast cancer cell lines. Chromatin-bound and soluble Pfn1 levels were quantified by western blotting. The effects of nuclear (nuclear localization sequence-Pfn1) and cytoplasmic (nuclear export sequence-Pfn1) localization on cell growth, DNA replication, and stemness were assessed using colony formation, Alamar blue fluorescence, replication protein A 32-kDa foci staining, and DNA fiber assays. Mouse xenografts of breast cancer cells were used to determine the effect of Pfn1 localization on tumor growth
resultsPfn1 expression was positively correlated with DNA replication, repair, p53, and MYC expression. Chromatin-bound Pfn1 was significantly degraded in breast cancer cell lines compared to that in non-cancerous MCF10a cells. Nuclear Pfn1 inhibited cell growth and DNA replication in SKBR3 cells, while cytoplasmic Pfn1 promoted cell survival and DNA replication in MCF10a cells. Loss of nuclear Pfn1 in SKBR3 cells inhibited their growth
conclusionOur findings revealed that nuclear Pfn1 acts as a tumor suppressor by inhibiting DNA replication and cell growth, while cytoplasmic Pfn1 promotes tumorigenesis by enhancing stemness and replication efficiency. These results highlight the dual role of Pfn1 in breast cancer progression, governed by its subcellular localization. They suggested that modulating Pfn1 nuclear-cytoplasmic shuttling may be a potential therapeutic strategy.
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.