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. Author manuscript; available in PMC: 2008 Jan 12.
Published in final edited form as: Cell. 2007 Jan 12;128(1):129–139. doi: 10.1016/j.cell.2006.11.039

Figure 7. NEDD4-1 RNAi inhibited xenotransplanted tumor growth in a PTEN-dependent manner.

Figure 7

(A) The human prostate cancer cell lines, DU-145 (PTEN-positive) and PC3 (PTEN-negative), were stably infected with NEDD4-1 RNAi and the control LacZ RNAi retroviruses. The infected cells were subcutaneously injected into athymic nude mice and the xenotransplanted tumor growth was measured, as described in Experimental Procedures.

(B) A Model for the potential function of NEDD4-1 in prostate tumorigenesis. After loss of one allel of PTEN, aberrant upregulation of NEDD4-1 function will further decrease PTEN protein level and thus accelerates cancer development. Upregulation of NEDD4-1 might lead to malignancy more rapidly than a complete loss of PTEN gene, because the latter will trigger INK4a and p53-dependent senescence (Chen et al., 2005). NEDD4-1 offers a new entry point for therapeutic intervention that could arrest tumorigenesis in cooperation with the senescence response.