The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Negative Regulation of Tumor Suppressor p53 by MicroRNA miR-504
Open accessAbstract
Summary Tumor suppressor p53 plays a central role in tumor prevention. p53 protein levels and activity are under a tight and complex regulation in cells to maintain the proper function of p53. microRNAs play a key role in the regulation of gene expression. Here we report the regulation of p53 through microRNA miR-504. miR-504 acts as a negative regulator of human p53 through its direct binding to two sites in p53 3′-UTR. Overexpression of miR-504 decreases p53 protein levels and functions in cells, including p53 transcriptional activity, p53-mediated apoptosis and cell cycle arrest in response to stress, and furthermore, promotes tumorigenecity of cells in vivo. These results demonstrate the direct negative regulation of p53 by miR-504 as a mechanism for p53 regulation in cells, which highlights the importance of microRNAs in tumorigenesis.
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Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 7×
“The tumor suppressor p53 plays a crucial role in maintaining genomic stability and preventing tumor formation (Levine et al., 2006; Vogelstein et al., 2000; Vousden and Prives, 2009).”
BackgroundInfluentialSelf-citationBlinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
Kastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047 · cited 1×
“It has been well established that p53 induces G1 arrest in cells in response to stress (Deng et al., 1995; Kastan et al., 1992).”
BackgroundRequirement for p53 and p21 to Sustain G 2 Arrest After DNA Damage
Bunz, F., Dutriaux, A., Lengauer, C., Waldman, T., Zhou, S., Brown, J. P., Sedivy, J. M., Kinzler, K. W., & Vogelstein, B. (1998) · Science · doi:10.1126/science.282.5393.1497 · Cited by 2,803
Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
Deng, C., Zhang, P., Wade Harper, J., Elledge, S. J., & Leder, P. (1995) · Cell · doi:10.1016/0092-8674(95)90039-x · Cited by 2,113
Feng, Z., Hu, W., de Stanchina, E., Teresky, A. K., Jin, S., Lowe, S., & Levine, A. J. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-4149 · Cited by 633
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Cited by
Cellular Senescence: Defining a Path Forward
Gorgoulis, V., Adams, P. D., Alimonti, A., Bennett, D. C., Bischof, O., Bishop, C., Campisi, J., Collado, M., Evangelou, K., Ferbeyre, G., et al. (2019) · Cell · doi:10.1016/j.cell.2019.10.005 · Cited by 3,225
Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype
Kumari, R., & Jat, P. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.645593 · Cited by 1,622
Lujambio, A., & Lowe, S. W. (2012) · Nature · doi:10.1038/nature10888 · Cited by 1,084
MicroRNAs in the p53 network: micromanagement of tumour suppression
Hermeking, H. (2012) · Nature Reviews Cancer · doi:10.1038/nrc3318 · Cited by 518
Tumour-associated mutant p53 drives the Warburg effect
Zhang, C., Liu, J., Liang, Y., Wu, R., Zhao, Y., Hong, X., Lin, M., Yu, H., Liu, L., Levine, A. J., et al. (2013) · Nature Communications · doi:10.1038/ncomms3935 · Cited by 434
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Metadata
- Authors
- Hu, W., Chan, C. S., Wu, R., Zhang, C., Sun, Y., Song, J. S., Tang, L. H., Levine, A. J., & Feng, Z.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 38
- Issue
- 5
- Pages
- 689-699
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W2005109475
- Cited by
- 313
- References
- 6
- FWCI
- 6.86
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Hu, W., Chan, C. S., Wu, R., Zhang, C., Sun, Y., Song, J. S., Tang, L. H., Levine, A. J., & Feng, Z. (2010). Negative Regulation of Tumor Suppressor p53 by MicroRNA miR-504. Molecular Cell. https://doi.org/10.1016/j.molcel.2010.05.027
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