Tomentosin induces apoptotic pathway by blocking inflammatory mediators via modulation of cell proteins in AGS gastric cancer cell line.

In this study, we investigated the in vitro effect of tomentosin on cell proliferation by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, reactive oxygen species by 2',7'-dichlorofluorescein diacetate staining assay, apoptosis (AO/EtBr, propidium iodide, and 4',6-diamidino-2-phenylindole staining, mitochondrial membrane potential), cell adherent, cell migration, inflammation, apoptosis, and oxidative stress from gastric cancer cells (GCCs) AGS. Upon their relative cell proliferative, inflammatory, and apoptotic molecular markers were analyzed by using the enzyme-linked immunosorbent assay and Western blot analysis method. Treatment with tomentosin (IC50  = 20 µM) significantly inhibited cell proliferation and oxidative stress-induced anti-cell proliferative (proliferating cell nuclear antigen and cyclin-D1) also regulated expression, drastically diminished tumor necrosis factor-α, nuclear factor-κB, interleukin-6, and interleukin-1β expression levels, significantly upregulated Bcl-2 and Bax expression. Thus, this tomentosin can significantly reduce GCC proliferation via cytotoxicity which is stimulated apoptosis markers via morphology staining changes and inhibitory inflammatory markers. The tomentosin-induced oxidative stress may be involved to stimulate apoptotic mechanisms via mitochondria-mediated signaling by the inhibition of inflammation. Taken together, our findings suggest a possible future use of chemotherapeutic agents for pharmacological benefits and as an anti-cancer treatment option.