Stachyose-induced apoptosis of Caco-2 cells via the caspase-dependent mitochondrial pathway

Abstract

Some studies have shown that stachyose, as prebiotics, can prevent indirectly colon cancer cell growth by promoting the proliferation of probiotics or producing beneficial materials in the intestine. However, its direct inhibitory effects on cancer cells are still unclear. Thus, this study aims to investigate the direct inhibitory effect of stachyose on human colon cancer cells and determine the molecular mechanism underlying this effect. The MTT assay was used to assess the inhibitory effect of stachyose on Caco-2 cells. Apoptosis and mitochondrial membrane potential (ΔΨm) measurements were analyzed using flow cytometry. The activities and mRNA expressions of caspases 3 and 9 were determined using caspase assay kits and quantitative real-time polymerase chain reaction. The apoptotic protein expressions of Bcl-2, Bax, and cytochrome C (Cyt C) were detected through western blotting. Results showed that stachyose inhibits Caco-2 cell proliferation and induces apoptosis in a dose-dependent manner. After pretreatment with 0.4, 0.8, 1.6 and 3.2 mg mL(-1) stachyose, cell inhibitory rates of 15.31% ± 3.20%, 28.45% ± 2.10%, 40.23% ± 5.70%, and 55.67% ± 4.50% were respectively obtained. Compared with the control, decreases in ΔΨm, increases in caspase 3 and 9 activities and mRNA expressions, down-regulation of Bcl-2 protein expression, up-regulation of the Bax protein and Cyt C release of Caco-2 cells were clearly observed upon exposure to different stachyose concentrations. The inhibitory mechanism of stachyose on Caco-2 cells involves the caspase-dependent mitochondrial apoptosis pathway.

Hydroxy-α-sanshool Possesses Protective Potentials on H2O2-Stimulated PC12 Cells by Suppression of Oxidative Stress-Induced Apoptosis through Regulation of PI3K/Akt Signal Pathway

“…* * P < 0:01 vs. the control group. 9 Oxidative Medicine and Cellular Longevity serine/threonine kinase activated by recruitment to the plasma membrane and is a key mediator of PI3K-mediated signal transduction [42,43]. As is shown in Figure 8, the direct results of PI3K phosphorylation is the phosphorylation of AKT, which further affects the expression of Bcl-2 and Bax proteins.…”

“…In addition, the PI3K/AKT pathway shows significant antioxidant activity in central and peripheral neurons and can be considered a potential therapeutic target for neurodegenerative diseases, participating in the cellular protective mechanism of ROS-induced cell damage [ 39 ]. AKT is a serine/threonine kinase activated by recruitment to the plasma membrane and is a key mediator of PI3K-mediated signal transduction [ 42 , 43 ]. As is shown in Figure 8 , the direct results of PI3K phosphorylation is the phosphorylation of AKT, which further affects the expression of Bcl-2 and Bax proteins.…”

Melittin induces human gastric cancer cell apoptosisviaactivation of mitochondrial pathway

“…When the transmembranous potential of the mitochondria declines, Cyt C located in the space within the mitochondrial membrane is released into the cytoplasm and forms a complex polymer with apoptotic enzyme activators [38] . The protein activates a caspase cascade reaction, which further activates downstream caspase-3 and other members of the caspase family, forming an Apaf-1 and procaspase 9 apoptosis body, and both are further combined with caspase-3 to induce apoptosis [39][40][41] . In this study, we found that the Cyt C protein release and cell apoptosis were increased as the concentration of melittin was elevated ( Figure 1B).…”

Antitumour effect of glucooligosaccharides obtained via hydrolysis of α-(1 → 3)-glucan from Fomitopsis betulina

“…In fact, the pro-apoptotic activity of oligosaccharides and low-molecular-weight α-glucans has been described in the literature. Huang et al [4] showed that oligosaccharides (stachyose) induced apoptosis and inhibited the growth of Caco-2 colorectal adenocarcinoma cells. In addition, an oligosaccharide isolated and purified from Bombyx batryticatus was found to induce apoptosis and cell cycle arrest in G 0 /G 1 and G 2 /M phases in HeLa cells [8].…”