Figure 2.

CCAT2 promotes tumor growth and metastasis. (A) CCAT2 increased subcutaneous tumor formation in a mouse xenograft model. Comparison was made between the empty vector and CCAT2 groups at the indicated weekly time points using the t-test. (B) HCT116 cells transduced with CCAT2 showed significantly higher migration ability, as measured by using a migration chamber. Data are presented as mean ± SEM from three independent experiments. (C) Knockdown of CCAT2 reduces invasion ability of KM12SM colon cancer cells. After treatment with CCAT2 siRNA (50 nM) for 24 h, cells were seeded onto an invasion assay chamber for 48 h, and invaded cells were stained and counted. (D) CCAT2 enhances liver metastasis in mice that were incubated by intrasplenic injection with HCT116 cells. A representative image of liver metastasis from the CCAT2 group is shown. (E) CCAT2 expression levels in Italian primary CRC samples from patients with metastasis (M1) were higher than those from without metastasis (M0). Comparison was made using the Mann-Whitney test. Data are presented as box-whisker plots. (F) Breast cancer patients with high CCAT2 had shorter metastasis-free survival. Kaplan-Meier analysis as a function of CCAT2 levels in 129 lymph node–positive breast cancer patients who received adjuvant combination chemotherapy with cyclophosphamide, methotrexate, and 5-fluorouracil. CCAT2 high level to normalizer, >0.0045; CCAT2 low level, ≤0.0045.