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There is growing evidence for the notion that certain alterations in tumor cells are not necessarily so-called “drivers” that initiate or maintain the neoplastic state. The idea that there are also “enablers” that facilitate or enable cancer cells to proliferate under conditions of stress has been gaining traction. This idea has great translational potential, as such factors can represent novel targets for therapeutic intervention. In PNAS, Bublik et al. (1) propose that the fibroblast growth factor 13 (FGF13) protein exerts just such effects during tumorigenesis. Intriguingly, the authors show that these effects are under the transcriptional regulation of the tumor suppressor p53. Understanding the molecular bases of this well-characterized role for p53 in human cancer has been an active area of research and remains elusive. The Bublik et al. study provides yet another possible mechanism: that p53 has the ability to dampen or down-regulate the activity of “enablers,” such as FGF13. FGF13 is a member of the FGF superfamily. Although it shares some homology to the well-studied members that interact with cell surface receptors, FGF13 is one of several that have not been implicated in playing such a role (2). Rather, this group, which includes FGF11–FGF14, all appear to have intracellular localization and functions (3). In the Bublik et al. study (1) the focus is on FGF13 and its role in the nucleolus. Data are presented in support of the idea that FGF13 down-regulates expression of ribosomal …

Tumor suppression by p53 involves inhibiting an enabler, FGF13