MicroRNAs in the miR-106b family regulate p21/CDKN1A and promote cell cycle progression
Open accessAbstract
microRNAs in the miR-106b family are overexpressed in multiple tumor types and are correlated with the expression of genes that regulate the cell cycle. Consistent with these observations, miR-106b family gain of function promotes cell cycle progression, whereas loss of function reverses this phenotype. Microarray profiling uncovers multiple targets of the family, including the cyclin-dependent kinase inhibitor p21/CDKN1A. We show that p21 is a direct target of miR-106b and that its silencing plays a key role in miR-106b-induced cell cycle phenotypes. We also show that miR-106b overrides a doxorubicin-induced DNA damage checkpoint. Thus, miR-106b family members contribute to tumor cell proliferation in part by regulating cell cycle progression and by modulating checkpoint functions.
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miR-106b targets several genes implicated in cell cycles, such as p21, E2F, TAF5-like RNA polymerase II, and PTEN.
“Previous studies have shown that miR-106b targets several genes implicated in cell cycles, such as cyclin-dependent kinase inhibitor 1A (p21), E2F transcription factor, TAF5-like RNA polymerase II, and phosphatase and tensin homolog (Ivanovska et al., 2008; Pichiorri et al., 2008; Poliseno et al., 2010; Trompeter et al., 2011).”
From miR-106b impairs cholesterol efflux and increases Aβ levels by repressing ABCA1 expression (2012) · cites this paper as Ivanovska et al., 2008
The Results identify p21/CDKN1A as a direct miR-106b target and report other likely cell-cycle-related targets. They do not identify TAF5-like RNA polymerase II or PTEN as targets; E2F appears in the references, but the Results say previously identified single targets were not regulated in this experimental system. Because the citations are not assigned to individual genes, this source supports only part of the cited list. (LLM, conf=0.87)
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- Authors
- Ivanovska, I., Ball, A. S., Diaz, R. L., Magnus, J. F., Kibukawa, M., Schelter, J. M., Kobayashi, S. V., Lim, L., Burchard, J., Jackson, A. L., Linsley, P. S., & Cleary, M. A.
- Affiliations
- Rosetta Inpharmatics LLC, Seattle, Washington 98109
- Corresponding author
- Ivanovska, Irena
- ORCID
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2008-04-01
- Volume
- 28
- Issue
- 7
- Pages
- 2167-2174
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC2268421
- OpenAlex
- W2100975741
- Cited by
- 561
- References
- 52
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 9 · 2023: 13 · 2022: 9 · 2021: 17 · 2020: 19 · 2019: 26 · 2018: 25 · 2017: 21 · 2016: 32 · 2015: 37 · 2014: 52 · 2013: 58 · 2012: 53
- FWCI
- 20.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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
- microRNA, CDKN1A/p21, cell cycle progression, cyclin-dependent kinase inhibitors, microRNA target regulation, tumor cell proliferation
- MeSH terms
- Breast, Cell Cycle, Cell Line, Transformed, DNA Damage, Doxorubicin, Female, Humans, Neoplasm Proteins, RNA, Messenger, RNA, Neoplasm, Genes, cdc, RNA Interference, RNA, Small Interfering, MicroRNAs, Cyclin-Dependent Kinase Inhibitor p21
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