Table I.
Condensin recruitment and activation of the UCC–MCD pathway in a panel of human cell lines with different p53 constitutions treated with NCS
| Cell lines | p53 status | Condensin recruitment and UCC |
MCD |
|---|---|---|---|
| HeLa | Inactivated | + | + |
| U2OSwt | Wild type | – | – |
| U20SshLacZ | Wild type | – | – |
| U20Sshp53 | Knocked down | – | – |
| 293T | Inactivated | + | + |
| HCT116wt | Wild type | – | – |
| HCT116p53−/− | Knocked out | + | + |
| MDA-MB-231 | Mutated | – | – |
| MDA-MB-435 | Mutated | – | – |
Cells were treated with ≥200 ng/ml NCS and examined for UCC and MCD at 24 and 72 h, respectively. In HEK 293T cells (293T), p53 is stabilized and inactivated by SV40 large T antigen (Ahuja et al., 2005). In HCT116 (p53−/−) cells, the TP53 gene encoding p53 was inactivated using homologous recombination (Bunz et al., 1998). In MDA-MB-231 and -435 cells, both TP53 alleles are inactivated by mutations (Gartel et al., 2003). In HeLa cells, p53 is inactivated by the HPV-E6 protein (Scheffner et al., 1990).