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Syringic acid induces apoptosis in human oral squamous carcinoma cells through mitochondrial pathway

BACKGROUND: Syringic acid (SA) has long been used as traditional medicine and is known to have antioxidant, hepatoprotective, neuroprotective and anticancer effects. Studies regarding the anticancer effect of SA against squamous carcinoma cell (SCC)-25, human oral SCC (OSCC) line has not been studie...

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Detalles Bibliográficos
Autores principales: Abijeth, Bhaskhar, Ezhilarasan, Devaraj
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer - Medknow 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7269318/
https://www.ncbi.nlm.nih.gov/pubmed/32508446
http://dx.doi.org/10.4103/jomfp.JOMFP_178_19
Descripción
Sumario:BACKGROUND: Syringic acid (SA) has long been used as traditional medicine and is known to have antioxidant, hepatoprotective, neuroprotective and anticancer effects. Studies regarding the anticancer effect of SA against squamous carcinoma cell (SCC)-25, human oral SCC (OSCC) line has not been studied. AIM: This study was aimed to evaluate the cytotoxic potentials of SA in SCC-25 cells. MATERIALS AND METHODS: Cytotoxic effect of SA was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenylte trazolium bromide assay, using concentrations of 25 and 50 μM/mL for 24 h. At the end of the treatment period, apoptotic markers such as caspase 3 and 9, bcl-2, bax and cytochrome c were evaluated by semiquantitative reverse transcription-polymerase chain reaction. SA-induced morphological changes were investigated by acridine orange/ethidium bromide dual staining. RESULTS: SA inhibited the proliferation and induced cytotoxicity in SCC-25 cells in a concentration-dependent manner. SA treatment caused apoptosis-related morphological changes as evidenced by the dual staining and the modulation of apoptotic marker gene expressions. SA treatments modulated bcl-2/bax homeostasis and increased the expressions of cytochrome c and caspases 3 and 9. CONCLUSION: SA specifically induces cell death and inhibits the proliferation in OSCC cells through intrinsic/mitochondrial apoptosis pathway, suggesting that SA may be an effective agent for the treatment of human OSCC.