The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.
p53: Protection against Tumor Growth beyond Effects on Cell Cycle and Apoptosis
Abstract
The tumor suppressor p53 has established functions in cancer. Specifically, it has been shown to cause cell-cycle arrest and apoptosis in response to DNA damage. It is also one of the most commonly mutated or silenced genes in cancer and for this reason has been extensively studied. Recently, the role of p53 has been shown to go beyond its effects on cell cycle and apoptosis, with effects on metabolism emerging as a key contributor to cancer growth in situations where p53 is lost. Beyond this, the role of p53 in the tumor microenvironment is poorly understood. The publication by Wang and colleagues demonstrates for the first time that p53 is a key negative regulator of aromatase and, hence, estrogen production in the breast tumor microenvironment. It goes further by demonstrating that an important regulator of aromatase, the obesity-associated and tumor-derived factor prostaglandin E2, inhibits p53 in the breast adipose stroma. This review presents these findings in the context of established and emerging roles of p53 and discusses possible implications for the treatment of breast cancer. Cancer Res; 75(23); 5001–7. ©2015 AACR.
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“Accumulated p53 is stabilized and activated through posttranslational modifications, including methylation, phosphorylation and acetylation,53 which regulate gene transcription and affect a series of signaling pathways involved in apoptosis, cell cycle arrest, senescence, autophagy, ferroptosis, cellular metabolism and the tumor immune microenvironment (TME)54–56 (Fig. 2).”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [56]
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2 retracted
Obesity Is Associated with Inflammation and Elevated Aromatase Expression in the Mouse Mammary Gland
Subbaramaiah, K., Howe, L. R., Bhardwaj, P., Du, B., Gravaghi, C., Yantiss, R. K., Zhou, X. K., Blaho, V. A., Hla, T., Yang, P., et al. (2011) · Cancer Prevention Research · doi:10.1158/1940-6207.capr-10-0381 · Cited by 363
RetractedSubbaramaiah, K., Morris, P. G., Zhou, X. K., Morrow, M., Du, B., Giri, D., Kopelovich, L., Hudis, C. A., & Dannenberg, A. J. (2012) · Cancer Discovery · doi:10.1158/2159-8290.cd-11-0241 · Cited by 244
RetractedHallmarks of Cancer: The Next Generation
Hanahan, D., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.02.013 · Cited by 66,590
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607
The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases.
Wade Harper, J. (1993) · Cell · doi:10.1016/0092-8674(93)90499-g · Cited by 5,651
In Vivo Activation of the p53 Pathway by Small-Molecule Antagonists of MDM2
Vassilev, L. T., Vu, B. T., Graves, B., Carvajal, D., Podlaski, F., Filipovic, Z., Kong, N., Kammlott, U., Lukacs, C., Klein, C., et al. (2004) · Science · doi:10.1126/science.1092472 · Cited by 4,661
The Biology of Cancer: Metabolic Reprogramming Fuels Cell Growth and Proliferation
DeBerardinis, R. J., Lum, J. J., Hatzivassiliou, G., & Thompson, C. B. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2007.10.002 · Cited by 4,088
Orimo, A., Gupta, P. B., Sgroi, D. C., Arenzana-Seisdedos, F., Delaunay, T., Naeem, R., Carey, V. J., Richardson, A. L., & Weinberg, R. A. (2005) · Cell · doi:10.1016/j.cell.2005.02.034 · Cited by 3,759
Live or let die: the cell's response to p53
Vousden, K. H., & Lu, X. (2002) · Nature Reviews Cancer · doi:10.1038/nrc864 · Cited by 3,192
Blinded 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
Cited by
Gérard, C., & Brown, K. A. (2018) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2017.09.014 · Cited by 136
Self-citationPresent and Future Perspective on PLK1 Inhibition in Cancer Treatment
Chiappa, M., Petrella, S., Damia, G., Broggini, M., Guffanti, F., & Ricci, F. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.903016 · Cited by 120
p53: from understanding its structure to advances in therapeutic targeting
Wang, W., Liu, X., Liu, H., Abolhassani, H., Yan, H., Zhang, H., & Wang, X. (2026) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02549-5 · Cited by 30
Self-citationWang, K., Liu, W., Xu, Q., Gu, C., & Hu, D. (2021) · Phytomedicine · doi:10.1016/j.phymed.2021.153553 · Cited by 28
Colonna, G. (2024) · Livers · doi:10.3390/livers4020016 · Cited by 7
Metadata
- Authors
- Wang, X., Simpson, E. R., & Brown, K. A.
- Venue
- Cancer Research
- Published
- 2015-11-30
- Volume
- 75
- Issue
- 23
- Pages
- 5001-5007
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2178157469
- Cited by
- 304
- References
- 65
- FWCI
- 8.71
- Type
- journal article
- Language
- en
- Open access
- closed
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