ArticleScientific reports2025
Cold atmospheric plasma restores fulvestrant sensitivity by inhibiting CCND3 in the drug-resistant breast cancer cells.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Cold atmospheric plasma (CAP) has demonstrated anti-proliferative activity in various cancer cells, yet its efficacy against drug-resistant cancer cells remains largely unexplored. This study investigates CAP's potential to restore drug sensitivity in fulvestrant-resistant breast cancer cells. Fulvestrant-resistant T47D/fulR and MCF-7/fulR cell lines were developed through 32-week drug exposure. CAP treatment effectively inhibited growth of both resistant cell lines and restored sensitivity to fulvestrant when used as pretreatment. Genome-wide expression analysis revealed that CAP significantly impacts ribosomal and mitochondrial components during resistance acquisition and treatment. The oncogene CCND3 emerged as a key contributor to drug resistance, being highly upregulated in resistant cells but downregulated following CAP treatment. Functional validation through CCND3 knockdown in both resistant cell lines induced increased apoptosis and extended G1 phase, confirming its critical role in resistance mechanisms. These findings demonstrate that CAP can revert fulvestrant-resistant breast cancer cells to a sensitive state by targeting CCND3 and modulating critical cellular pathways, suggesting promising therapeutic potential for overcoming drug resistance in breast cancer treatment.
Indexed as
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.