Research Paper Volume 13, Issue 4 pp 5034—5054

Transcriptional dysregulation of TRIM29 promotes colorectal cancer carcinogenesis via pyruvate kinase-mediated glucose metabolism


Figure 4. TRIM29 promotes the growth and metastasis of CRC in vivo. (A, B) Mice were subcutaneously injected with HT29 cells (A) or HCT116 cells (B) in both side of the top back (lenti-NC in the left and lenti-shTRIM29/lenti-pTRIM29 in the right). Tumor weight of both lenti-NC and lenti-shTRIM29/lenti-pTRIM29 cell-derived tumors in nude mice was measured two weeks later (n=10). (C) Representative IHC staining of TRIM29, Ki67 and PKM1 in two mice with HT29 and HCT116 xenografts derived from lenti-NC and lenti-shTRIM29/lenti-pTRIM29 cells. (DG) Mice were injected with HT29 or HCT116 cells (2*106 cells in 0.1 ml) via tail vein; lenti-NC group (n=5), lenti-shTRIM29/lenti-pTRIM29 group (n=5). (D, F) Rate of lung metastasis after tail injection. (E, G) Rate of liver metastasis after tail injection. The statistical analysis was performed using two-tailed Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001.