ArticleJournal of ovarian research2026
SCHEMBL4796824: a multifaceted antitumor agent targeting microtubule dynamics, DNA damage, and Wnt/β-catenin signaling in ovarian cancer cells.
Article in Journal of ovarian research, 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
12 authors.
Funding
Abstract
SCHEMBL4796824, a BPR0L075 derivative with antitumor properties, targets tubulin's colchicine binding site and induces DNA damage response in ovarian cancer. Cell counting kit-8 (CCK-8) assay confirmed its anti-proliferative effects, while wound healing and transwell assays demonstrated inhibition of migration and invasion. Flow cytometry showed G2 phase arrest. Molecular docking and immunofluorescence revealed microtubule depolymerization via tubulin binding, analogy with BPR0L075. Real-time qPCR and western blot analysis indicated activation of ATM/Chk2 and ATR/Chk1 pathways by SCHEMBL4796824. Senescence-associated-β-galactosidase (SA-β-gal) staining showed senescence induction. Molecular docking studies suggested potential interaction with CTNNB1. Crucially, functional assays demonstrated inhibition of the Wnt/β-catenin pathway, as evidenced by downregulation of β-catenin and c-MYC. The β-catenin agonist reversed SCHEMBL4796824-induced DNA damage and senescence, establishing a causal link to the observed phenotypes. Notably, these effects were more pronounced in c-MYC amplified SK-OV-3 cells. In summary, SCHEMBL4796824 disrupts the canonical Wnt/β-catenin signaling, inducing DNA damage, and inhibits the Wnt/β-catenin/c-MYC axis, triggering cellular senescence in a pathway-dependent manner, hinting at a novel therapeutic approach.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.