RESUMO
Objective: To establish the glioma-bearing nude mouse models, and to investigate the effect of HOXA4 on the growth of glioma U251 cells in vivo and its regulatory effect on the Wnt/β-catenin sgnal pathway and its mechanism Methods: The glioma U251 cell line stably transfected with HOXA4 siRNA (si-HOXA4) and the U251 cell line stably transfected with blank vector (si-NC) were established by lentivirus transfection The U251, si-NC, and si-HOXA4 cells were respectively inoculated under the skin of the neck and back of the BALB/c nude mice to establish the glioma-bearing nude mouse models named as control group, si-NC group, and si-HOXA4 group. The tumorigenesis of nude mice in various groups were observed and the tumor growth curve was drawn. The tumor tssue was stripped after the mice were sacrificed on the 21 th day, and the volume and wght of tumor were measured; the relative mRNA expresson amounts of HOXA4, CTNNB1, and Gsk3fS in tumor tssue of the nude mice in various groups were detected by qRT-PCR method; the expresson levels of HOXA4, β-catenin, Gsk3β, CyclinD1, and P53 proteins in tumor tissue of the nude mice in various groups were detected by immunohistochemstry (IHC) method. Results: Compared with si-NC group and control group, the volume and wght of tumor of the nude mice in si-HOXA4 group were gnificantly decreased (P<0. 05). The relative expresson amount of HOXA4 mRNA and the expresson level of HOXA4 protein in si-HOXA4 group were gnificantly lower than those in the other groups (P<0. 05). Compared with si-NC group and control group, the relative expresson amount of CTNNB1 mRNA and the expresson levels of β-catenin and CyclinDl proteins in si-HOXA4 group were significantly decreased (P<0. 05), and the expresson levels of Gsk3β and P53 proteins were gnificantly increased (P<0. 05). Conclusion: Inhibition of HOXA4 expresson in human glioma U251 cells can regulate the expressons of CyclinDl and P53 through Wnt/-catenin gnal pathway in vivo, thus inhibiting the tumor growth of glioma-bearing nude mice.