ArticleHeliyon2025
Proliferation and migration inhibition of adenoid cystic carcinoma cells through autophagy suppression via GLUT1 knockdown.
Article in Heliyon, 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.
- PIEZO2 in tumors: from mechanobiological switches to activity-targeted therapies.Journal of experimental & clinical cancer research : CR · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple studies have demonstrated a significant association between glucose transporter-1 (GLUT1) and the development and recurrence of adenoid cystic carcinoma (ACC). In this study, we investigated the impact of GLUT1 knockdown on adenoid cystic carcinoma. Our findings revealed that hypoxic conditions promoted the progression and autophagy of SACC83 and SACC-LM cell lines, an effect that was mitigated by GLUT1 knockdown. In vivo experiments showed that the combination of lentivirus-delivered GLUT1 shRNA and autophagy inhibitor chloroquine (CQ) produced the most substantial reduction in tumor volume, weight, Ki67 expression, and autophagy in tumor tissues. In conclusion, hypoxia facilitates ACC progression by upregulating GLUT1 expression. The suppression of GLUT1 expression and autophagy effectively inhibited ACC cell proliferation both
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Registered trials
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