ArticleCancer prevention research (Philadelphia, Pa.)2010
A novel mechanism of indole-3-carbinol effects on breast carcinogenesis involves induction of Cdc25A degradation.
Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 34 citations in OpenAlex.
- Identification and validation of an ECERIFERUM2- LIKE gene controlling cuticular wax biosynthesis in cabbage (Brassica oleracea L. var. capitata L.).TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2021Article
- Global Survey of the Full-Length Cabbage Transcriptome (International journal of molecular sciences · 2021Article
- Genome-wide identification and characterization of non-specific lipid transfer proteins in cabbage.PeerJ · 2018Article
- Ciclopirox inhibits cancer cell proliferation by suppression of Cdc25A.Genes & cancer · 2017Article
- Oxidative Stress: A Promising Target for Chemoprevention.Current pharmacology reports · 2016Article
- Review
- 3,3'-Diindolylmethane inhibits breast cancer cell growth via miR-21-mediated Cdc25A degradation.Molecular and cellular biochemistry · 2011Article
- Cdc25A regulates matrix metalloprotease 1 through Foxo1 and mediates metastasis of breast cancer cells.Molecular and cellular biology · 2011Article
- Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells.Clinical epigenetics · 2011Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
The natural compound indole-3-carbinol (I3C; found in vegetables of the genus Brassica) is a promising cancer prevention or therapy agent. The cell division cycle 25A (Cdc25A) phosphatase is overexpressed in a variety of human cancers and other diseases. In the present study, I3C induced degradation of Cdc25A, arrest of the G(1) cell cycle, and inhibition of the growth of breast cancer cells. We also showed that the Ser124 site of Cdc25A, which is related to cyclin-dependent kinase 2, is required for I3C-induced degradation of Cdc25A in breast cancer cells, and that interruption of the ATM-Chk2 pathway suppressed I3C-induced destruction of Cdc25A. Our in vivo studies of different mutated forms of Cdc25A found that the mutation Cdc25A(S124A) (Ser124 to Ala124), which confers resistance to I3C-induced degradation of Cdc25A, attenuated I3C inhibition of breast tumorigenesis in a mouse xenograft model. The present in vitro and in vivo studies together show that I3C-induced activation of the ATM-Chk2 pathway and degradation of Cdc25A represent a novel molecular mechanism of I3C in arresting the G(1) cell cycle and inhibiting the growth of breast cancer cells. The finding that I3C induces Cdc25A degradation underscores the potential use of this agent for preventing and treating cancers and other human diseases with Cdc25A overexpression.
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