Proliferation and migration inhibition of adenoid cystic carcinoma cells through autophagy suppression via GLUT1 knockdown.

Heliyon

State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.

Published: February 2025

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 and .

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894374PMC
http://dx.doi.org/10.1016/j.heliyon.2025.e42894DOI Listing

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