ArticleJournal of experimental & clinical cancer research : CR2026
Methyl-cantharidimide suppresses cyclin-dependent kinase 1 (CDK1) and induces oxeiptosis in liver cancer.
Article in Journal of experimental & clinical cancer research : CR, 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
6 authors.
Funding
Abstract
backgroundMethyl-cantharidimide (MCA), a cantharidin (CTD) analog, has been approved in China for the clinical treatment of liver cancer. Previous studies have shown that MCA can induce both apoptosis and cell cycle arrest in cancer cells. However, the precise molecular mechanisms underlying its anticancer activity remain largely unclear.
methodsThe effects of MCA were evaluated in liver cancer cell lines using colony formation assays. Bioinformatic analysis was performed to explore molecular mechanisms, with validation via immunoblotting and immunofluorescence. Reactive oxygen species (ROS) production was measured to assess oxidative stress induction. A 3D multicellular tumor spheroid (MCTS) model was used to mimic tumor-like in vitro conditions, and a HepG2 xenograft mouse model was employed to investigate in vivo efficacy.
resultsMCA significantly inhibited colony formation in liver cancer cells. Bioinformatic profiling suggested that downregulation of cyclin-dependent kinase 1 (CDK1) may mediate MCA-induced cell cycle arrest, which was confirmed by suppressed CDK1 expression in both immunoblotting and immunofluorescence assays. MCA also increased intracellular ROS levels. Further analyses revealed that MCA-induced apoptosis occurred through a ROS-dependent oxeiptosis pathway, rather than the conventional caspase-dependent route. In the MCTS model, MCA maintained its cytotoxicity, demonstrating efficacy under more physiologically relevant conditions. In the in vivo xenograft mouse model, MCA treatment led to a significant reduction in tumor size.
conclusionsMCA exerts anticancer effects in liver cancer cells by inducing cell cycle arrest via CDK1 downregulation and promoting apoptosis through a ROS-dependent oxeiptosis pathway. These findings provide mechanistic insight into MCA’s antitumor activity and support its potential as a therapeutic agent for liver cancer.
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.