ArticleHeliyon2024
Quercetin represses cholesterol metabolism and mitigates resistance to cisplatin in oral squamous cell carcinoma by regulating AGR2/AKT/SREBP2 axis.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed.
- Cisplatin resistance in oral squamous cell carcinoma: mechanisms, reversal strategies, and emerging technologies.Frontiers in physiology · 2026Review
- The regulatory role and mechanism of energy metabolism and immune response in head and neck cancer.Genes & diseases · 2025Review
- Agr2 in cancer and beyond: unraveling its role during protein synthesis, ER stress, and as a predictive biomarker.Molecular and cellular biochemistry · 2025Review
- Synergistic chemotherapy and immunomodulatory effects of Quercetin in cancer: a review.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: This study aimed to explore the effects of quercetin on cholesterol metabolism and cisplatin sensitivity in oral squamous cell carcinoma (OSCC) cell line (CAL27) and investigate the potential molecular mechanisms. Methods: CAL27 cells were exposed to quercetin or cisplatin after upregulation or downregulation of AGR2. The expression of proteins and genes associated with cholesterol metabolism were assessed. The levels of cholesterol and LDL were also measured, and the cisplatin sensitivity of CAL27 cells was analyzed. Results: RNA high-throughput sequencing revealed that after treatment with quercetin, the expression of AGR2 was significantly reduced in cisplatin-resistant CAL27 cells (CAL-27R), which was associated with lipid metabolism. AGR2 deletion ameliorated but its overexpression exacerbated cisplatin resistance and cholesterol metabolism, evidenced by changes in SQLE, HMGCS, LDLR, and n-SREBP2 expression and cholesterol and LDL levels. Moreover, AGR2 promoted cisplatin resistance by activating the AKT signaling pathway and enhancing SREBP2-mediated cholesterol metabolism. Quercetin increased cisplatin sensitivity by repressing cholesterol metabolism but suppressed the AGR2/AKT/SREBP2 signaling pathway in a concentration-dependent manner. These effects were partly reversed by AGR2 overexpression and AKT activation. Conclusion: Our findings demonstrated that quercetin inhibits cholesterol metabolism and cisplatin resistance in CAL27 cells by modulating the AGR2/AKT/SREBP2 axis.
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