The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Loss of the miR-21 allele elevates the expression of its target genes and reduces tumorigenesis
Open accessAbstract
MicroRNA 21 (miR-21) is overexpressed in virtually all types of carcinomas and various types of hematological malignancies. To determine whether miR-21 promotes tumor development in vivo, we knocked out the miR-21 allele in mice. In response to the 7,12-dimethylbenz[ a ]anthracene (DMBA)/12- O -tetradecanoylphorbol-13-acetate mouse skin carcinogenesis protocol, miR-21 -null mice showed a significant reduction in papilloma formation compared with wild-type mice. We revealed that cellular apoptosis was elevated and cell proliferation was decreased in mice deficient of miR-21 compared to wild-type animals. In addition, we found that a large number of validated or predicted miR-21 target genes were up-regulated in miR-21 -null keratinocytes, which are precursor cells to skin papillomas. Specifically, up-regulation of Spry1 , Pten , and Pdcd4 when miR-21 was ablated coincided with reduced phosphorylation of ERK, AKT, and JNK, three major downstream effectors of Ras activation that plays a predominant role in DMBA-initiated skin carcinogenesis. These results provide in vivo evidence that miR-21 exerts its oncogenic function through negatively regulating its target genes.
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Cites
Mammalian microRNAs predominantly act to decrease target mRNA levels
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MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts
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RAS oncogenes: the first 30 years
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“A family of GDP-GTP exchange factors (GEFs) for the Ral small GTPases (RalGDS, for instance) represents the third family of Ras effectors (27).”
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Self-citationModulation of K-Ras-Dependent Lung Tumorigenesis by MicroRNA-21
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“Second, in the Olson model, miR-21 loss does not cause significant change in cellular apoptosis and proliferation in lung tissues and tumors; in our model, increased apoptosis was observed in miR-21-null cells and skin tissues, along with Ta b le 1.”
BackgroundResultInfluential
Cited by
The functions and regulation of the PTEN tumour suppressor
Song, M. S., Salmena, L., & Pandolfi, P. P. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3330 · Cited by 1,926
MicroRNAs en route to the clinic: progress in validating and targeting microRNAs for cancer therapy
Kasinski, A. L., & Slack, F. J. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3166 · Cited by 936
Au Yeung, C. L., Co, N.-N., Tsuruga, T., Yeung, T.-L., Kwan, S.-Y., Leung, C. S., Li, Y., Lu, E. S., Kwan, K., Wong, K.-K., et al. (2016) · Nature Communications · doi:10.1038/ncomms11150 · Cited by 774
Self-citationTurning 21: Induction of miR-21 as a Key Switch in the Inflammatory Response
Sheedy, F. J. (2015) · Frontiers in Immunology · doi:10.3389/fimmu.2015.00019 · Cited by 496
Adult-specific functions of animal microRNAs
Sun, K., & Lai, E. C. (2013) · Nature Reviews Genetics · doi:10.1038/nrg3471 · Cited by 334
Metadata
- Authors
- Ma, X., Kumar, M., Choudhury, S. N., Becker Buscaglia, L. E., Barker, J. R., Kanakamedala, K., Liu, M.-F., & Li, Y.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2011-06-06
- Volume
- 108
- Issue
- 25
- Pages
- 10144-10149
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2051584801
- Cited by
- 214
- References
- 14
- FWCI
- 7.75
- Type
- journal article
- Language
- en
- Open access
- green
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- Ma, X., Kumar, M., Choudhury, S. N., Becker Buscaglia, L. E., Barker, J. R., Kanakamedala, K., Liu, M.-F., & Li, Y. (2011). Loss of the miR-21 allele elevates the expression of its target genes and reduces tumorigenesis. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1103735108
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