ArticleEuropean journal of medical research2025
DACT1 inhibits cuproptosis and promotes cell malignancy via activation of PI3K/AKT signaling in laryngeal squamous cell carcinoma.
Article in European journal of medical research, 2025. 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
No grant is acknowledged in the PubMed record.
Abstract
backgroundLaryngeal cancer has one of the highest mortality rates of all head and neck cancers. DACT1 is a cuproptosis-related gene in laryngeal cancer and serves as a risk factor for patient prognosis. This study aimed to investigate the effects of DACT1 on the malignant behavior and cuproptosis of laryngeal squamous cell carcinoma (LSCC) cells.
methodsDACT1 expression in LSCC cells was measured using RT-qPCR and western blotting. To establish cuproptosis cell model, TU212 and TU686 cells were incubated with elesclomol (20 nM) and CuCl
resultsDACT1 expression was upregulated in LSCC cells. DACT1 knockdown inhibited LSCC cell proliferation, migration, and invasion. DACT1 depletion enhanced cuproptosis, as evidenced by more pronounced decreases in cell viability, increased intracellular copper concentration and ROS levels, upregulation of HSP70, and downregulation of LIAS. Notably, treatment with the cuproptosis inhibitor tetrathiomolybdate reversed the pro-cuproptosis effects induced by DACT1 silencing. Furthermore, the silencing of DACT1 inactivated the PI3K/AKT signaling, as shown by reduced ratios of p-PI3K/PI3K and p-AKT/AKT. Conversely, DACT1 overexpression activated the PI3K/AKT pathway, an effect that was abolished by LY294002. Moreover, LY294002 reversed the promoting effects of DACT1 on LSCC cell malignancy and its inhibitory effects on cuproptosis. In contrast, activation of the PI3K signaling by 740Y-P reversed the enhancement of cuproptosis caused by DACT1 deficiency.
conclusionDACT1 promotes the malignant behavior of LSCC cells and suppresses cuproptosis by activating the PI3K/AKT signaling.
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.