ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Twist1 silencing suppresses triple-negative breast cancer progression by reducing RNF40 transcription.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- E3 ubiquitin ligase RNF40: Structure, function and its context‑dependent roles in tumorigenesis (Review).Oncology reports · 2026Review
- Stage-Specific Regulation of Ubiquitination Modifications and Prospects for Targeted Therapy in Triple-Negative Breast Cancer.Oncology research · 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
RING finger protein 40 (RNF40) has been reported to play a key role in cancer development, progression, and metastasis, and may act as an oncogene in triple-negative breast cancer (TNBC). Herein, the oncogenic role and upstream molecular mechanism of RNF40 in TNBC progression were investigated. Detection of mRNA and protein levels was performed using qRT-PCR, western blotting, and immunohistochemical (IHC) staining, respectively. Functional experiments were conducted using colony formation, EdU, flow cytometry, wound healing, transwell, and tube formation assays in vitro, and xenograft mouse models in vivo. The interaction between Twist-related protein 1 (Twist1) and RNF40 was verified by using RNA immunoprecipitation and dual-luciferase reporter assays. RNF40 was highly expressed in TNBC patients and showed a good diagnostic value for TNBC. Its expression was also increased in TNBC cell lines and the silencing of RNF40 suppressed TNBC cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and angiogenesis as well as induced cell apoptosis in vitro, and hampered TNBC growth and EMT in vivo. Mechanically, Twist1 promoted RNF40 transcription. TNBC tissues and cells also showed a higher Twist1 expression. The deficiency of Twist1 led to a decrease in RNF40 expression, and restrained TNBC cell growth, migration, invasion, EMT, and angiogenesis by regulating RNF40. Twist1 contributed to TNBC cell growth, migration, invasion, EMT, and angiogenesis by promoting RNF40 transcription, suggesting a new insight into the pathogenesis of TNBC.
Indexed as
Identifiers
40679592What Socratic 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 Socratic graph.