Mutant and wild-type Ras: co-conspirators in cancer

Abstract

Although the functional interplay between mutant and wild-type Ras in driving tumor initiation and growth has been described, a clear picture of the precise ramifications and mechanisms of this association remains elusive, sometimes with conflicting conclusions. A report in this issue of Cancer Discovery tackles this question, which may have important implications for therapeutic strategies to block mutant Ras for cancer treatment.

Figure 1

Functional interplay between WT and mutant Ras. Shown in this figure are the signaling interactions between mutationally activated K-Ras and WT H-Ras and N-Ras. Similar interactions are also seen human tumor cells harboring mutated H-Ras or N-Ras and the remaining two WT Ras isoforms. siRNA silencing of either mutant (*) KRAS or concurrently WT HRAS and NRAS reduces tumor cell proliferation.