Figure 5.

miR-101 overexpression or CXCR7 knockdown suppressed tumor growth and metastasis in vivo. Severe combined immune deficiency (SCID) mice were injected subcutaneously or intravenously with Molt 4-luc cells that were infected with a control lentivirus (Lenti-pGCsi or Lenti-pLKO.1) or a recombinant lentivirus expressing an miR-101 precursor (Lenti-pGCsi-miR-101) or shCXCR7 (Lenti-shCXCR7). (A) In vivo luciferase image for the detection of xenograft growth. (B) Tumor weight was measured after 50 days of implantation. (C) Terminal transferase-mediated dUTP nick end labeling (TUNEL) assay was conducted to detect the percentage of apoptotic cells. (D) Numbers of metastatic foci in the lungs from various groups at 5 weeks after tail vein injection. mRNA (E) and protein (F) levels of CXCR7 in the tumor tissues were assessed by qPCR and Western blot assays. GAPDH and β-actin were used as the loading controls, respectively. (G) Representative Western blot results of p-STAT3, STAT3, cyclin D1, Bcl-xl, Bcl-2, MMP-2, and MMP-9 in the tumor tissues. β-Actin was used as a loading control. All data are shown as mean ± SD of three separate experiments. *p < 0.05, **p < 0.01 versus Lenti-pGCsi or Lenti-pLKO.1 group.