HMGA1 is required for migration, invasion, anchorage-independent cell growth, and limiting dilution tumorigenicity.

<p>(A) Transfection with an shRNA knockdown vector for <i>HMGA1</i> in highly aggressive, poorly differentiated human colon cancer cells (HCT116 and SW480) results in a significant decrease in HMGA1 protein. (B) Migration and invasion were assessed in control (dark bars) and HMGA1 knock-down (open bars) colon cancer cells (HCT116 and SW480). The graph shows the mean ± the standard deviation from 2 experiments done in triplicate. (p-values determined by student's t-tests are shown). (C) Anchorage-independent cell growth in soft agar in control (dark bars) and HMGA1 knock-down (open bars) colon cancer cells (HCT116 and SW480). All foci >50 µm were counted. The bar graph shows the mean ± the standard deviation from two experiments done in triplicate. (p-values determined by student's t-tests are shown). (D) The table shows that knock-down of HMGA1 blocks tumor formation at limiting dilutions. The photograph shows representative nude mice 4 weeks following injection with control or HMGA1 knock-down in HCT116 cells (10⁵/injection). No tumors formed in the HMGA1 knock-down cells.