Abstract:

Objective　To elucidate the effect and mechanism of astragalus polysaccharide (AP) on SCC-25 xenograft tumor model mice in oral squamous cell carcinoma (OSCC) cell line.　Methods　The xenograft tumor model was established by subcutaneous injection of oral squamous cell carcinoma cell line SCC-25, and the xenograft tumor BALB/c nude mice models were randomly divided into 4 groups: a control group (cTRL), an AP low-dose group (AP 10 mg), an AP medium-dose group (AP 25 mg) and an AP high-dose group (AP 50 mg) for subsequent experiments. After treatment with AP, the tumor volume and survival rate of mice were measured. The expression of Ki67 and vascular endothelial growth factor (VEGF) were detected by immunohistochemistry. Apoptosis of xenograft tumor cells was detected by TUNEL assay. Protein expression of JAK2/STAT3 pathway members was detected by Western blot.　Results　Compared with the control group, the tumor volume of the low, medium and high-dose groups were decreased significantly (P<0.01), and the survival rate of the mice was increased significantly in AP treated groups (P<0.01). In addition, the expression levels of Ki67 and VEGF were decreased significantly (P<0.01), and the phosphorylation levels of JAK2/STAT3/c-myc were significantly inhibited (P<0.01).　Conclusion　AP inhibits the growth of SCC-25 xenograft tumors in a dose-dependent manner; particularly, AP increases the survival rate of xenograft tumor mice, and down-regulates the expression levels of Ki67 and VEGF and the phosphorylation level of JAK2/STAT3/c-myc. AP may inhibit oral squamous cell line SCC-25 xenograft tumor by inhibiting JAK2/STAT3/c-myc signaling pathway.