ArticleCell communication and signaling : CCS2025
C/EBPβ increases tumor aggressiveness by enhancing KIFC1 expression in androgen receptor negative triple negative breast cancer.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Integrated bulk, single-cell and spatial transcriptomic analyses identify KIFC1 as a driver of malignant progression in lung adenocarcinoma.Molecular biology reports · 2026Article
- Glucocorticoid-Induced Proteome and Phosphoproteome Changes in Breast Cancer Cell Lines.Journal of proteome research · 2026Article
- Lipid Droplets in Cancer: New Insights and Therapeutic Potential.International journal of molecular sciences · 2026Review
- Integrating molecular targeting and immune modulation in triple-negative breast cancer: from mechanistic insights to therapeutic innovation.Frontiers in immunology · 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
10 authors.
Funding
Abstract
Quadruple-negative breast cancers (also known as AR-triple negative (TN) BC) lack the expression of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), and androgen receptor (AR). AR-TNBC exhibits aggressive characteristics and a poor prognosis. Because of the lack of expression of therapeutic targets, limited therapeutic options exist for patients with AR-TNBC. Hence, new therapeutic targets and risk-predictive biomarkers are required for patients with AR-TNBC. In this study, we investigated the role of kinesin-like protein 1 (KIFC1) in AR-TNBC. We found that C/EBPβ binds to the KIFC1 promoter and induces its expression in the AR-TNBC cells. Notably, AR status was negatively correlated with KIFC1 levels. We also found that AR transcriptionally repressed the transcription factor C/EBPβ, which regulates the expression of KIFC1. The lack of AR expression in AR-TNBC led to C/EBPβ upregulation, thereby enhancing KIFC1 expression. Moreover, upregulation of KIFC1 in AR-TNBC increased cancer cell proliferation and promoted epithelial-mesenchymal transition (EMT), contributing to the aggressive characteristics of AR-TNBC. Inhibiting KIFC1 using the small molecule inhibitor CW069 significantly reduced tumor volume in mice bearing AR-TNBC xenografts, but not in those with triple-negative breast tumors. These data suggest that upregulation of C/EBPβ and KIFC1 contributes to the aggressive characteristics and poor prognosis of AR-TNBC, providing strong evidence that targeting KIFC1 using kinesin inhibitors could be a viable therapeutic approach for patients with AR-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.