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. 2013 Oct 18;21(1):146–160. doi: 10.1038/cdd.2013.141

Figure 6.

Figure 6

PTEN-controlled tumorigenesis is dependent upon p34 and NEDD4-1. (a) Western blot analyses of PTEN, NEDD4-1, p34, and Ras expression in p53−/− MEFs that were infected with PTEN, NEDD4-1, or p34 revealed that p34 expression decreases PTEN expression and increases NEDD4-1 expression. (b) Colony-forming assays revealed that the overexpression of NEDD4-1 increases cellular transformation by Ras in p53−/− MEFs. Representative photos are shown in the right-hand panel. The data represent the means±S.D.'s of at least three independent experiments (**P<0.01) (c) Western blot analysis of PTEN, NEDD4-1, p34, and Ras expression in NEDD4-1-knockdown p53−/− MEFs infected with Ras and PTEN or NEDD4-1 revealed that p34 does not enhance PTEN levels in the absence of NEDD4-1. (d) Colony-forming assays confirmed that cell transformation is inhibited in NEDD4-1-knockdown p53−/− MEFs. Representative photos are shown in the right-hand panel. The data represent the means±S.D.'s of at least three independent experiments. (e) Ubiquitination assays in intact cells revealed that p34 does not enhance NEDD4-1-mediated PTEN poly-ubiquitination in NEDD4-1-knockdown p53−/− MEFs. (f) Colony-forming assays (lower panel) and western blot analyses (upper panel) revealed that PTEN knockdown potentiates cellular transformation in Ras-infected p53−/− MEFs. The data represent the means±S.D.'s of at least three independent experiments (**P<0.01)