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. 2011 Apr;13(4):348–357. doi: 10.1593/neo.101580

Figure 6.

Figure 6

Introduction of a constitutively active K-RasV12 oncogene and shRNA-mediated depletion of TP53 induces the emergence of trisomy 20. (A) Knockdown of TP53 and expression of K-RasV12 in HCEC 1CT+7. (B) Karyotypic analysis reveals +20 in 7 of 35 cells analyzed by GTG banding. No +20 cells were detected in diploid HCECs under the same conditions. Neither knockdown of TP53 nor expression of K-RasV12 alone was sufficient to induce +20 in HCEC 1CT+7. The addition of an extra chromosome 20 has no effect on (C) anchorage-dependent (adherent culture) and (D) -independent (soft agar) clonogenicity. HCT-116 colon cancer cells were used as a positive control for anchorage independent growth. All columns represent mean ± SEM.