Intact p53-Dependent Responses in miR-34–Deficient Mice
Open accessAbstract
MicroRNAs belonging to the miR-34 family have been proposed as critical modulators of the p53 pathway and potential tumor suppressors in human cancers. To formally test these hypotheses, we have generated mice carrying targeted deletion of all three members of this microRNA family. We show that complete inactivation of miR-34 function is compatible with normal development in mice. Surprisingly, p53 function appears to be intact in miR-34-deficient cells and tissues. Although loss of miR-34 expression leads to a slight increase in cellular proliferation in vitro, it does not impair p53-induced cell cycle arrest or apoptosis. Furthermore, in contrast to p53-deficient mice, miR-34-deficient animals do not display increased susceptibility to spontaneous, irradiation-induced, or c-Myc-initiated tumorigenesis. We also show that expression of members of the miR-34 family is particularly high in the testes, lungs, and brains of mice and that it is largely p53-independent in these tissues. These findings indicate that miR-34 plays a redundant function in the p53 pathway and suggest additional p53-independent functions for this family of miRNAs.
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Results of experiments that used overexpression or knockdown of miR-34 or lincRNA-p21 barely overlapped with those that used knockout mice.
“For example, results of experiments that used overexpression or knockdown of miR-34 or lincRNA-p21124, 125 barely overlapped with those that used knockout mice.128, 129”
From Census and evaluation of p53 target genes (2017) · cites this paper as [128]
A recent mir-34-knockout mouse model suggests caution; the mir-34 family does not have a substantial effect on p53 tumour suppressor functions in vivo.
“These studies have revealed that the mir-34 family does not have a substantial effect on p53 tumour suppressor functions in vivo54.”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [54]
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- Authors
- Concepcion, C. P., Han, Y.-C., Mu, P., Bonetti, C., Yao, E., D'Andrea, A., Vidigal, J. A., Maughan, W. P., Ogrodowski, P., & Ventura, A.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Ventura, Andrea
- Venue
- PLoS Genetics
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-07-26
- Volume
- 8
- Issue
- 7
- Pages
- e1002797
- ISSN
- 1553-7390 (ISSN-L)
- 1553-7404
- PMC
- PMC3406012
- OpenAlex
- W2063878022
- Cited by
- 197
- References
- 67
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 10 · 2021: 15 · 2020: 7 · 2019: 11 · 2018: 11 · 2017: 22 · 2016: 26 · 2015: 23 · 2014: 33 · 2013: 17 · 2012: 5
- FWCI
- 8.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS Genetics (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Keywords
- miR-34, microRNA, p53 pathway, p53-independent function, tumor suppressor microRNA, cell cycle arrest, apoptosis, carcinogenesis, c-Myc, tissue-specific gene expression, testis, lung, brain
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Cells, Cultured, Fibroblasts, Humans, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Apoptosis, Mice, Knockout, MicroRNAs, Cell Proliferation, Mice, Cell Cycle Checkpoints
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