ArticleFrontiers in oncology2026
Quercetin selectively targets gingival squamous cell carcinoma through apoptosis induction, autophagy suppression, DNA damage, and chemosensitization.
Article in Frontiers in oncology, 2026. 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Oral squamous cell carcinoma (OSCC) remains a major clinical challenge due to high recurrence rates, chemotherapy resistance, and severe treatment-related toxicity. Although quercetin, a naturally occurring flavonoid, has demonstrated anti-cancer properties, its selective activity and molecular mechanisms in distinct OSCC subtypes remain insufficiently characterized. Methods: In this study, we investigated the anti-tumor effects of quercetin in human gingival squamous cell carcinoma (Ca9-22), tongue carcinoma (SCC-9 and CAL-27), and non-malignant oral epithelial (GMSM-K) cells. Results: Quercetin (0-100 µM) selectively reduced the viability, proliferation, and clonogenic potential of gingival carcinoma cells while exerting limited cytotoxicity toward non-malignant oral epithelial cells, suggesting a favorable therapeutic index. Mechanistically, quercetin induced apoptosis through modulation of intrinsic and extrinsic apoptotic pathways, suppressed autophagy, reduced oxidative stress, promoted DNA damage, and inhibited migratory and metastatic potential. Transcriptomic profiling identified several apoptosis-related genes modulated by quercetin, including CASP9 and BIRC3, whose elevated expression was associated with improved overall survival in head and neck squamous cell carcinoma datasets. In addition, quercetin enhanced the anti-proliferative effects of cisplatin and 5-fluorouracil, supporting its potential role as a chemosensitizing agent in OSCC therapy. Molecular docking and molecular dynamics simulations further demonstrated stable interactions between quercetin and apoptosis- and DNA damage-related proteins, including CASP9, H2AX, and BIRC3. Conclusions: Collectively, these findings identify quercetin as a selective multi-target anti-cancer compound capable of modulating apoptosis, autophagy, oxidative stress, DNA damage, and metastatic pathways in gingival squamous cell carcinoma. These data support the translational potential of quercetin as a complementary strategy to enhance chemotherapy efficacy in oral cancer.
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.