The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Caspase-3 Promotes Genetic Instability and Carcinogenesis
Open accessAbstract
Summary Apoptosis is typically considered an anti-oncogenic process since caspase activation can promote the elimination of genetically unstable or damaged cells. We report that a central effector of apoptosis, caspase 3, facilitates, rather than suppresses, chemical and radiation-induced genetic instability and carcinogenesis. We found that a significant fraction of mammalian cells treated with ionizing radiation can survive, despite caspase 3 activation. Moreover, this sublethal activation of caspase 3 promoted persistent DNA damage and oncogenic transformation. In addition, chemically-induced skin carcinogenesis was significantly reduced in mice genetically deficient in caspase 3. Furthermore, attenuation of Endo G activity significantly reduced radiation-induced DNA damage and oncogenic transformation, identifying Endo G as a downstream effector of caspase 3 in this pathway. Our findings suggest that rather than acting as a broad inhibitor of carcinogenesis, caspase 3 activation may contribute to genome instability and play a pivotal role in tumor formation following damage.
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DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139
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Genetic instabilities in human cancers
Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1998) · Nature · doi:10.1038/25292 · Cited by 4,168 · cited 1×
“Chromosome instability is key characteristic of cancer cells (Lengauer et al., 1997, 1998).”
The Bcl2 family: regulators of the cellular life-or-death switch
Cory, S., & Adams, J. M. (2002) · Nature Reviews Cancer · doi:10.1038/nrc883 · Cited by 4,032
Endonuclease G is an apoptotic DNase when released from mitochondria
Li, L. Y., Luo, X., & Wang, X. (2001) · Nature · doi:10.1038/35083620 · Cited by 1,787
Heavy ion carcinogenesis and human space exploration
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Mitochondrial endonuclease G is important for apoptosis in C. elegans
Parrish, J., Li, L., Klotz, K., Ledwich, D., Wang, X., & Xue, D. (2001) · Nature · doi:10.1038/35083608 · Cited by 427
Cited by
Regulation of apoptosis in health and disease: the balancing act of BCL-2 family proteins
Singh, R., Letai, A., & Sarosiek, K. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0089-8 · Cited by 2,111
The Role of Cancer-Associated Fibroblasts and Fibrosis in Liver Cancer
Affo, S., Yu, L.-X., & Schwabe, R. F. (2017) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-052016-100322 · Cited by 757
A fate worse than death: apoptosis as an oncogenic process
Ichim, G., & Tait, S. W. G. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2016.58 · Cited by 451
Modes of Regulated Cell Death in Cancer
Koren, E., & Fuchs, Y. (2021) · Cancer Discovery · doi:10.1158/2159-8290.cd-20-0789 · Cited by 371
Mitochondrial permeabilization engages NF-κB-dependent anti-tumour activity under caspase deficiency
Giampazolias, E., Zunino, B., Dhayade, S., Bock, F., Cloix, C., Cao, K., Roca, A., Lopez, J., Ichim, G., Proïcs, E., et al. (2017) · Nature Cell Biology · doi:10.1038/ncb3596 · Cited by 258
Metadata
- Authors
- Liu, X., He, Y., Li, F., Huang, Q., Kato, T. A., Hall, R. P., & Li, C.-Y.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 58
- Issue
- 2
- Pages
- 284-296
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W2002049273
- Cited by
- 263
- References
- 6
- FWCI
- 9.39
- Type
- journal article
- Language
- en
- Open access
- green
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