ArticleBMC cancer2024
A novel role for nonactin: interfering with G-quadruplex in RET-driven medullary thyroid cancer.
Article in BMC cancer, 2024. 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.
- Anticancer Activity of Endophytic Bacterial Extracts from Potentilla supina in HepG2 and HCT116 Cells.Current microbiology · 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
8 authors.
Funding
Abstract
backgroundMedullary Thyroid Carcinoma (MTC) is closely associated with mutations in the RET proto-oncogene, placing the activated RET protein at the center of MTC pathogenesis. Existing therapeutic solutions, primarily tyrosine kinase inhibitors such as selpercatinib, vandetanib, and cabozantinib, have shown moderate efficacy but are accompanied by increased risks of side effects and resistance. This study unveils a promising avenue using nonactin, a compound historically recognized for its antibacterial properties, targeting the G-quadruplex interactions within the RET proto-oncogene.
methodIn this research, high-throughput screening was conducted using a luciferase reporter-based cellular assay. The MTC TT cell line was treated with nonactin for 24 and 48 h. Immunoblotting and RT-PCR were employed to measure the protein and RNA levels of RET and its downstream stream proteins. Binding to the G-Quadruplex was assessed using melting curves and Circular Dichroism. The cell cycle was analyzed using FACS, and caspase activity was measured to indicate the activation of apoptosis.
resultsNonactin was identified to significantly reduce luciferase activity driven by the RET promoter. A deeper exploration revealed nonactin's remarkable selectivity against tumor cell lines harboring RET mutations, effectively inducing apoptosis. Nonactin was also found to bind to the G-quadruplex region on RET.
conclusionThe findings highlight the compound's therapeutic potential, emphasizing its mechanism of inducing apoptosis in active mutant RET cell lines by interacting with G-quadruplex structures. This novel insight opens avenues for a potentially effective treatment for MTC, potentially bypassing the challenges associated with current TKIs.
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.