ArticleCancer cell international2025
Taurochenodeoxycholic acid suppresses the progression of glioblastoma via HMGCS1/HMGCR/GPX4 signaling pathway in vitro and in vivo.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Taurochenodeoxycholic acid alleviates MPPIBRO neuroscience reports · 2026Article
- Cholesterol metabolism and cancer: Molecular mechanisms, immune regulation and an epidemiological perspective (Review).International journal of molecular medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Glioblastoma multiforme (GBM) is the foremost prevalent and highly aggressive intracranial malignancy, which urgently needs safer and more efficacious therapeutic strategies. Our research aimed to investigate the impact and the underlying mechanism of Taurochenodeoxycholic acid (TCDCA) on GBM. In this study, we explored the suppressive effect of TCDCA in vitro by qualification of proliferation and migration assays and flow cytometry, and subsequently predicted the potential anti-GBM mechanism of TCDCA by mRNA sequencing and the following rescue experiments. An orthotopic GBM model in C57BL/6 mice further demonstrated the anti-GBM mechanism of TCDCA. In vitro experiments verified that TCDCA inhibited the growth and migration of GBM cells and induced cell cycle arrest at the G2/M phase. Subsequent mechanism investigations showed that upregulation of HMGCS1 and HMGCR and downregulation of glutathione peroxidase-4 (GPX4) was observed in GBM cells by TCDCA treatment. Notably, inhibitory effects of proliferation and migration as well as induction of ferroptosis by TCDCA were partially restored by Simvastatin (SIN), a competitive HMGCR inhibitor. Furthermore, TCDCA showed an anti-GBM effect in an orthotopic transplantation model in vivo. TCDCA impedes GBM progression by virtue of this intricately orchestrated molecular cascade, through HMGCS1/HMGCR/GPX4 signaling axis, thus unveiling a novel therapeutic avenue warranting further scrutiny in the treatment landscape of GBM.
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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.