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 µmol/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 µmol/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.