Figure 4.
Knockdown of lncRNA XIST expression inhibits tumor growth and metastasis in vivo. (a) Knockdown of lncRNA XIST expression significantly inhibited tumor growth of HCT116 cells in nude mouse model. The tumor volume and tumor weight formed by HCT116 sh-XIST cells was significantly less than that of HCT116 sh-NC cells; the mean tumor volume was 356and 743 mm3 for the HCT116/sh-XIST and HCT116/sh-NC groups, respectively, and the mean tumor weight was 0.75 and 0.38 g for the HCT116/sh-XIST and HCT116/sh-NC groups, respectively (*P<0.05). (b) Of the mice, 91.6% developed tumors when injected with 2.0 × 105HCT116 sh-NC cells. The tumor incidence was 63.6% when mice were injected with 2.0 × 105 HCT116 sh-XIST cells (group 1); the tumor incidence was 54.5% when mice were injected with 1.0 × 105 sh-NC cells; the tumor incidence was 27.2% when mice were injected with 1.0 × 105 cells in the sh-XIST group (group 2); the tumor incidence was 36.3% and 0% when the mice were injected with 1.0 × 104 cells of sh-NC and sh-XIST, respectively (group 3). (c) Real-time PCR analysis showed that knockdown of lncRNA XIST significantly decreased the expression of lncRNA XIST in tumor tissues taken from the nude mice (*P<0.05). (d) Immunohistochemistry analysis showed that knockdown of lncRNA XIST significantly reduced Ki-67 expression. (e) Knockdown of lncRNA XIST significantly reduced the macrometastases in the liver. Of the 11 mice in the sh-NC group, 6 formed macroscopic liver metastases, whereas only 1 of 11 mice in the sh-XIST group formed macroscopic liver metastases. (f) The mean micro lung metastatic nodules were 2.6 and 7.9 for the HCT116/sh-XIST and HCT116/sh-NC groups, respectively, and the mean micro liver metastatic nodules were 1.3 and 6.5 for the HCT116/sh-XIST and HCT116/sh-NC groups, respectively (*P<0.05). Error bars represent the mean±S.D. values