ArticleOTO open
Targeting Stearoyl-CoA Desaturase 1 Through PI3K-AKT-mTOR Signaling in Head and Neck Squamous Cell Carcinoma.
Article in OTO open. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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
3 citing papers in PubMed.
- Based on artificial intelligence-assisted generation and in-depth in-silico evaluation of potential inhibitors targeting Stearoyl-CoA desaturase 1 (SCD-1).Scientific reports · 2026Article
- The Interaction of PI3K/AKT/mTOR Pathway with the Tumor Microenvironment: A Dual Engine Driving Breast Cancer Progression and Reshaping Treatment Strategies.Cancer management and research · 2026Review
- Conventional and alternative approaches for targeting PIK3CA and PTEN alterations in head and neck, breast, and other cancers.Advances in biological regulation · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Stearoyl-coenzyme A desaturase 1 (SCD1) is a key enzyme in fatty acid metabolism and has been implicated in cancer progression, including head and neck squamous cell carcinoma (HNSCC). The phosphoinositide 3-kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) signaling pathway is a critical regulator of cellular metabolism and survival in cancer. This study investigates the crosstalk between SCD1 inhibition and the PI3K-AKT-mTOR pathway, highlighting the therapeutic potential of targeting SCD1 in HNSCC. Study Design: Basic science. Setting: Laboratory. Methods: Four HNSCC cell lines were utilized to evaluate the relationship between SCD1 and the mTOR signaling pathway. Cell viability was assessed following treatment with various mTOR inhibitors. The effect of AKT-mTOR signaling on SCD1 expression was examined through pharmacological inhibition and gene silencing approaches. Additionally, the impact of SCD1 knockdown on cell proliferation and survival was analyzed. Results: mTOR inhibitors significantly reduced HNSCC cell viability and downregulated SCD1 expression in a dose-dependent manner. Inhibition of AKT, a key upstream effector of mTOR, also suppressed SCD1 expression, suggesting that SCD1 is regulated through the PI3K-AKT-mTOR axis. Silencing SCD1 independently impaired cancer cell growth and enhanced the cytotoxic effects of mTOR inhibitors, indicating a synergistic anticancer effect. Conclusion: SCD1 is a downstream target of the PI3K-AKT-mTOR pathway and contributes to HNSCC cell survival. Dual targeting of SCD1 and the mTOR signaling pathway represents a promising therapeutic strategy for HNSCC treatment. Further investigation is warranted to explore the clinical potential of SCD1 inhibitors in combination with mTOR-targeted therapies.
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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.