ArticleScientific reports2017
Oleic acid induces apoptosis and autophagy in the treatment of Tongue Squamous cell carcinomas.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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72 citing papers in PubMed, 156 citations in OpenAlex.
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- Perilipin2-dependent lipid droplets accumulation promotes metastasis of oral squamous cell carcinoma via epithelial-mesenchymal transition.Cell death discovery · 2025Article
- Article
- The effect of extracellular vesicles derived from oral squamous cell carcinoma on the metabolic profile of oral fibroblasts.Frontiers in molecular biosciences · 2025Article
- Oleic Acid Inhibits SDC4 and Promotes Ferroptosis in Lung Cancer Through GPX4/ACSL4.The clinical respiratory journal · 2024Article
- DPP3 promotes breast cancer tumorigenesis by stabilizing FASN and promoting lipid synthesis.Acta biochimica et biophysica Sinica · 2024Article
- Composite Hydrogel with Oleic Acid-Grafted Mesoporous Silica Nanoparticles for Enhanced Topical Delivery of Doxorubicin.Gels (Basel, Switzerland) · 2024Article
- The lipid basis of cell death and autophagy.Autophagy · 2024Review
- Chemical Analysis and Biological Activities of Extracts Isolated from SymbioticLife (Basel, Switzerland) · 2024Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oleic acid (OA), a main ingredient of Brucea javanica oil (BJO), is widely known to have anticancer effects in many tumors. In this study, we investigated the anticancer effect of OA and its mechanism in tongue squamous cell carcinoma (TSCC). We found that OA effectively inhibited TSCC cell proliferation in a dose- and time-dependent manner. OA treatment in TSCC significantly induced cell cycle G0/G1 arrest, increased the proportion of apoptotic cells, decreased the expression of CyclinD1 and Bcl-2, and increased the expression of p53 and cleaved caspase-3. OA also obviously induced the formation of autolysosomes and decreased the expression of p62 and the ratio of LC3 I/LC3 II. The expression of p-Akt, p-mTOR, p-S6K, p-4E-BP1 and p-ERK1/2 was significantly decreased in TSCC cells after treatment with OA. Moreover, tumor growth was significantly inhibited after OA treatment in a xenograft mouse model. The above results indicate that OA has a potent anticancer effect in TSCC by inducing apoptosis and autophagy via blocking the Akt/mTOR pathway. Thus, OA is a potential TSCC drug that is worthy of further research and development.
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