title: Evaluation of the antineoplastic activity of gallic acid in oral squamous cell carcinoma under hypoxic conditions.
abstract: The purpose of the current study was to develop and test a theoretical model that could explain the mechanism of action of gallic acid (GA) in the oral squamous cell carcinoma context for the first time. The theoretical model was developed using bioinformatics and interaction network analysis to evaluate the effect of GA on oral squamous cell carcinoma. In a second step to confirm theoretical results, migration, invasion, proliferation, and gene expression (Col1A1, E-cadherin, HIF-1α, and caspase-3) were performed under normoxic and hypoxic conditions. Our study indicated that treatment with GA resulted in the inhibition of cell proliferation, migration, and invasion in neoplastic cells. Observation of the molecular mechanism showed that GA upregulates E-cadherin expression and downregulates Col1A1 and HIF-1α expression, suggesting that GA might be a potential anticancer compound. In conclusion, the present study demonstrated that GA significantly reduces cell proliferation, invasion, and migration by increasing E-cadherin and repressing Col1A1.
authors: Departments of aDentistry bBiology, Universidade Estadual de Montes Claros cInstitute of Agricultural Sciences, Food Engineering College, Universidade Federal de Minas Gerais (UFMG), Montes Claros, Minas Gerais dDepartment of Oral Diagnosis, Oral Pathology Division, Piracicaba Dental School, University of Campinas, Piracicaba, Sao Paulo, Brazil eTexas Tech University Health Science Center, Lubbock, Texas, USA.
authors: Talita A
authors: TA
authors: Guimaraes
authors: Lucyana C
authors: LC
authors: Farias
authors: Carlos A
authors: CA
authors: Fraga
authors: John D
authors: JD
authors: Feltenberger
authors: Geraldo A
authors: GA
authors: Melo
authors: Ricardo D
authors: RD
authors: Coletta
authors: Sergio H
authors: SH
authors: Souza Santos
authors: Alfredo M B
authors: AM
authors: de Paula
authors: Andre L
authors: AL
authors: Guimaraes
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D015820:Cadherins / Q000378:metabolism; D002294:Carcinoma, Squamous Cell / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D053148:Caspase 3 / Q000378:metabolism; D015687:Cell Hypoxia; D045744:Cell Line, Tumor / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D024042:Collagen Type I / Q000378:metabolism; D000090602:Collagen Type I, alpha 1 Chain; D005707:Gallic Acid / Q000494:pharmacology*; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D008954:Models, Biological; D009062:Mouth Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D009361:Neoplasm Invasiveness
chemical_list: D000970:Antineoplastic Agents; D015820:Cadherins; D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D005707:Gallic Acid; D053148:Caspase 3