ArticleNeuromolecular medicine2025
Longikaurin A - Mediated Regulation of ROS/JNK Signaling Counteracts Epithelial-Mesenchymal Transition in Glioblastoma.
Article in Neuromolecular medicine, 2025. 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
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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
1 citing paper in PubMed.
- STIM/Orai-Mediated Store-Operated CaCells · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is a highly aggressive brain tumor characterized by rapid proliferation, therapy resistance, and extensive invasion, largely driven by epithelial-mesenchymal transition (EMT). Longikaurin A (LK-A), a natural kaurane diterpenoid, has demonstrated promising anti-cancer properties, yet its role in EMT regulation within GBM remains unclear. This study aimed to systematically investigate the inhibitory effects of LK-A on TGF-β1-induced EMT and to elucidate the underlying molecular mechanisms contributing to its anti-invasive potential in GBM. LK-A inhibited EMT-associated phenotypic changes, including reduced expression of mesenchymal markers (N-cadherin, Vimentin) and increased expression of epithelial markers (ZO-1, Occludin), alongside suppression of key EMT transcription factors (Snail, Twist1). Functionally, LK-A impaired EMT-induced cell migration, invasion, and glioma stem cell-like traits, evidenced by decreased gliosphere formation and downregulation of stemness markers such as Sox2 and Oct4. Mechanistic analyses revealed that LK-A triggered reactive oxygen species (ROS) accumulation, leading to the activation of the JNK/p38 MAPK signaling cascade. Pharmacological inhibition of JNK or ROS scavenging reversed the anti-EMT effects of LK-A, confirming that EMT suppression is mediated through ROS-dependent JNK activation. In vivo, LK-A significantly suppressed tumor growth, EMT marker expression, and stemness in xenograft models. Collectively, these findings identify LK-A as a potent regulator of EMT and glioma stemness via ROS/JNK signaling. This work provides new mechanistic insight into the anti-tumor effects of LK-A and highlights its potential as a promising therapeutic strategy for combating GBM aggressiveness.
Indexed as
Identifiers
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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 OpenQuestion graph.