Figure 5: Truncated APC in colon cancer cells is functional.

(a) Silencing of mutated APC in colon cancer cells increases AXIN2 expression. Schematic representation of the APC mutant proteins that are present in various colon cancer cell lines. All mutated APC proteins lack the SAMP (serine alanine methionine proline) repeats attributed to Axin binding. HT29 cells express the longest form of APC (1,555 aa); it retains all 15 AARs, as well as three of the seven 20 AARs, all of which are responsible for β-catenin binding/degradation. The indicated colon cancer cells were transfected with CTNNB1 or APC siRNAs for 72 h. Relative expression of the indicated mRNAs was determined by quantitative PCR. Data from three to four independent experiments are shown as mean±s.e.m. (b) β-Catenin binds to the main components of the destruction complex in colon cancer cells. The indicated cell lines were subjected to immunoprecipitation with anti-β-catenin antibody. Regardless of the extent of APC truncation, β-catenin co-immunoprecipitated APC, Axin1 and GSK3β. Western blottings are shown as representative of three independent experiments using the indicated antibodies.