A microRNA component of the p53 tumour suppressor network
Open accessAbstract
A global decrease in microRNA (miRNA) levels is often observed in human cancers, indicating that small RNAs may have an intrinsic function in tumour suppression. To identify miRNA components of tumour suppressor pathways, we compared miRNA expression profiles of wild-type and p53-deficient cells. Here we describe a family of miRNAs, miR-34a-c, whose expression reflected p53 status. Genes encoding miRNAs in the miR-34 family are direct transcriptional targets of p53, whose induction by DNA damage and oncogenic stress depends on p53 both in vitro and in vivo. Ectopic expression of miR-34 induces cell cycle arrest in both primary and tumour-derived cell lines, which is consistent with the observed ability of miR-34 to downregulate a programme of genes promoting cell cycle progression. The p53 network suppresses tumour formation through the coordinated activation of multiple transcriptional targets, and miR-34 may act in concert with other effectors to inhibit inappropriate cell proliferation.
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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 [124]
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- Authors
- He, L., He, X., Lim, L. P., de Stanchina, E., Xuan, Z., Liang, Y., Xue, W., Zender, L., Magnus, J., Ridzon, D., Jackson, A. L., Linsley, P. S., Chen, C., Lowe, S. W., Cleary, M. A., & Hannon, G. J.
- Affiliations
- Howard Hughes Medical Institute (US)
- Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
- Corresponding author
- Cleary, Michele A.
- Hannon, Gregory J.
- ORCID
- Venue
- Nature
- Published
- 2007-06-06
- Volume
- 447
- Issue
- 7148
- Pages
- 1130-1134
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC4590999
- OpenAlex
- W2144154026
- Cited by
- 2,692
- References
- 31
- Citations by year
- 2026: 30 · 2025: 44 · 2024: 49 · 2023: 61 · 2022: 85 · 2021: 104 · 2020: 116 · 2019: 106 · 2018: 113 · 2017: 163 · 2016: 161 · 2015: 188 · 2014: 255 · 2013: 228 · 2012: 244
- FWCI
- 60.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Cancer Institute (P01CA087497, K99CA126186, P01CA013106, P30CA008748)
- 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
- p53, microRNA, miR-34, transcriptional regulation, cell cycle arrest, cell proliferation, DNA damage response, miRNA target genes, p53-deficient cells
- MeSH terms
- Animals, Cell Cycle, Cell Division, Cell Line, DNA Damage, Gene Expression Regulation, Substrate Specificity, Transcription, Genetic, Tumor Suppressor Protein p53, MicroRNAs, Mice
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