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Syringic acid regulates suppression of the STAT3/JNK/AKT pathway via inhibition of human ovarian teratoma cancer cell (PA‐1) growth—in vitro study
Author(s) -
Yang Lina,
Qu Changhong,
Jin Jiaxi,
Yang Hong,
Pei Lipeng
Publication year - 2021
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22776
Subject(s) - protein kinase b , pi3k/akt/mtor pathway , downregulation and upregulation , stat3 , apoptosis , cancer research , cyclin d1 , cell growth , viability assay , cell cycle , cyclin e , cyclin dependent kinase 2 , chemistry , biology , microbiology and biotechnology , signal transduction , biochemistry , gene
Among the various gynaecological cancers, ovarian cancer (OC) is the third most severe cancer worldwide affecting women. Syringic acid (SRA) exhibits several hypoglycaemia, antioxidant, and anti‐inflammatory properties. The study aimed to examine the proapoptotic activities of SRA on OC in PA‐1 cells. SRA has been shown to decrease cell viability, increase the rate of cell apoptosis, and cause mitochondrial membrane potential to dissipate and induce over‐accumulation of intracellular reactive oxygen species in PA‐1 cells after 24 h of exposure. We examined the anticancer efficacy of SRA with its responsible molecular mechanism in the PA‐1 cell lines of human OC. In a dose‐dependent manner, SRA substantially suppressed cell proliferation and migration. SRA exhibited significant downregulation of cyclins including CDK2, CDK4, and Cyclin D1 responsible for cell‐cycle regulation. The apoptosis‐mediated anticancer activity was mainly mediated through caspase‐3, caspase‐8, caspase‐9 and Bax upregulation, and Bcl‐2 downregulation. We report that SRA significantly inhibits the expression of signal transducer and activator of transcription 3 (STAT3), c‐Jun N‐terminal kinase (JNK), P65, and protein kinase B (AKT) pathways. These findings depict the effective inhibition of STAT3, p38, and AKT expression by SRA, making it a potential therapeutic candidate for human OC.