Abstract
Unmet Expectations: miR-34 Plays No Role in p53-Mediated Tumor Suppression In Vivo
Highlights
In vivo modeling of tumor suppressor p53 functions and regulation has a history of unexpected and even enigmatic outcomes [1], despite the status of p53 as the most frequently mutated gene or dysfunctional pathway in human cancers [2,3]
Multiple in vitro analyses suggested that microRNA-34 family members are important players in a p53-regulated network of genomic surveillance [12,13,14,15,16,17] (Table 1)
These studies strongly supported the view that p53 response to multiple stimuli depended on miR-34, and that ectopic expression of miR-34 was sufficient to elicit p53 response, consistent with miR-34 functioning as a bonafide tumor suppressor
Summary
In vivo modeling of tumor suppressor p53 functions and regulation has a history of unexpected and even enigmatic outcomes [1], despite the status of p53 as the most frequently mutated gene or dysfunctional pathway in human cancers [2,3]. As reported by Concepcion et al in this issue of PLoS Genetics [11], expectations built on cell-based studies of p53 response are again unrealized in mouse models. Previous reports show that p53 directly activates miR-34a/b/c expression and, dependent on cellular context, they act downstream of p53 in mediating cell cycle arrest or apoptosis [29].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
