ArticleACS omega2025
The C2 Domain of PKC‑δ as a Dominant-Negative Modulator of Breast Cancer Cell Survival and Chemosensitivity.
Article in ACS omega, 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.
- Modelling the Full-Length Inactive PKC-δ Structure to Explore Regulatory Accessibility and Selective Targeting Opportunities.Pharmaceuticals (Basel, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mounting evidence implicates Protein Kinase C-δ (PKC-δ) in breast cancer progression and therapy resistance. PKC-δ is activated by the second messenger diacylglycerol or by proteolytic cleavage, both of which expose the kinase's catalytic site and allow substrate phosphorylation. Furthermore, the C2 domain of PKC-δ regulates the kinase by mediating intra and intermolecular protein-protein interactions. Here, we investigated the autonomous effects of the PKC-δ C2 domain in two breast cancer cell lines, representing hormone-dependent and triple-negative breast cancer. A myc-tagged PKC-δ C2 domain (myc-δC2) was stably overexpressed in MCF-7 and MDA-MB-468 cells, and its effects on cell viability, apoptosis, and proliferation were assessed. myc-δC2 expression reduced cell viability and increased apoptosis in both cell lines. In MCF-7 cells, but not in MDA-MB-468 cells, G2/M arrest and increased cell size were observed upon myc-δC2 expression. Under oxidative (H
Identifiers
What 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.