Exopolysaccharide of Antarctic bacterium Pseudoaltermonas sp. S-5 induces apoptosis in K562 cells

• Exopolysaccharide (PEP) inhibited the proliferation of K562 cells.
• PEP induced apoptosis through intrinsic pathway in K562 cells.
• Calcium signaling partially participated in the PEP-induced cell death.

The aim of this study was to investigate the anticancer activity of exopolysaccharide (PEP) of Antarctic bacterium Pseudoaltermonas sp. S-5 and elucidate the underlying molecular mechanisms. PEP significantly inhibited the growth of human leukemia K562 cells. Results of morphological characterization showed that PEP-treated cells displayed typical morphological characteristics of apoptosis such as condensation of chromatin and formation of apoptotic bodies. Flow cytometry analyses and colorimetric assay demonstrated that PEP induced collapse of mitochondrial membrane potential and activation of caspase-9, which indicated that intrinsic apoptotic signaling pathway was involved in apoptosis induced by PEP in K562 cells. Western blot analysis showed that PEP increased the ratio of Bax/Bcl-2. In addition, calcium signal might contribute to the cytotoxicity of PEP against K562 cells. These findings suggest that PEP may be potentially effective drug against human leukemia.