Antiproliferative and pro‑apoptotic effects of Cyclocarya paliurus polysaccharide and X‑ray irradiation combination on SW480 colorectal cancer cells.

The anti-hyperglycemic effects of Cyclocarya paliurus polysaccharide (CPP) have attracted increasing attention; however, limited research has been conducted on the potential effects of CPP on inhibiting tumor growth. The present study aimed to investigate the functions of CPP in combination with X-ray irradiation on colorectal cancer cells and the underlying mechanisms. SW480 cells were treated with various concentrations of CPP for 24, 48 and 72 h to determine cell viability using a Cell Counting Kit-8 assay. Then, the cells were divided into four groups as follows: Control, CPP (100 mu mol/l), 8 Gy and CPP + 8 Gy. The proliferation and apoptosis, and colony formation of cells were detected using flow cytometry and plate clone formation assays, respectively. Reverse transcription-quantitative PCR and western blot analyses were conducted to determine the expression of proliferation and apoptosis-associated, and PI3K/Akt signaling-associated genes. Treatment with 75 mu mol/l CPP for 48 h significantly decreased cell viability compared with untreated cells. CPP in combination with 8 Gy X-ray treatment significantly promoted the induction of apoptosis, and suppressed cell proliferation and clone formation compared with the control, CPP and 8 Gy groups. The detection of mRNA and protein expression levels by reverse transcription-PCR and western blotting demonstrated that CPP in combination with 8 Gy not only significantly decreased the expression of proliferation marker protein Ki-67, p53 and Bcl-2, but also upregulated the expression of cleaved caspase-3 and Bax, compared with the control. In addition, CPP and 8 Gy combined significantly attenuated the phosphorylation of PI3K and Akt. The present study demonstrated that the combination of CPP with X-ray irradiation suppressed SW480 cell proliferation and promoted cell apoptosis compared with the control, CPP and 8 Gy groups. The underlying mechanisms may involve inhibition of PI3K/Akt signaling.