ArticleMolecular biology reports2026
Melatonin inhibits malignant biological behaviors in carboplatin-resistant ovarian cancer cells: elucidating the potential molecular mechanisms.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
backgroundThe role of melatonin (MLT) in modulating malignant phenotypes of carboplatin (CBP)-resistant ovarian cancer (OC) cells remains unexplored. This study therefore aimed to investigate effects of MLT on malignant biological behaviors in CBP-resistant OC cells and to preliminarily delineate underlying molecular mechanisms.
methodsCBP-resistant A2780 and SKOV3 cell lines were first established, and their resistance index (RI) was determined by CCK-8 assay. Subsequently, effects of MLT were systematically evaluated: cell proliferation was assessed by CCK-8 assay; cell cycle distribution and apoptosis were analyzed by flow cytometry; and cell invasion and migration capabilities were examined using Transwell chambers. The potential mechanism by which MLT modulates malignant biological behaviors in CBP-resistant OC cells was elucidated through mRNA sequencing and bioinformatics analyses.
resultsCBP-resistant OC cell lines were successfully established. We demonstrated that MLT effectively suppressed key malignant phenotypes of CBP-resistant OC cells, including proliferation, cell cycle progression, invasion, and migration, while promoting apoptosis (P < 0.05). Transcriptomic analyses demonstrated that MLT upregulated 548 genes and downregulated 119 genes in A2780/CBP cells, and upregulated 70 genes and downregulated 232 genes in SKOV3/CBP cells. Notably, a common set of 26 differentially expressed genes (DEGs) was consistently identified in both resistant cell lines. These shared DEGs were significantly enriched in the GO term “negative regulation of canonical Wnt signaling pathway” and KEGG pathway “amphetamine addiction”.
conclusionsMLT inhibited malignant biological behaviors of CBP-resistant OC cells. The underlying mechanism likely involved the “negative regulation of canonical Wnt signaling pathway” (GO term) and “amphetamine addiction” (KEGG pathway).
Indexed as
Identifiers
41989617What 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.