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Increased susceptibility to carcinogen-induced mammary tumors in MMTV-Cdc25B transgenic mice
1Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University, 701 West 168th Street, New York, NY 10032, USA.
Abstract:
Cdc25 phosphatases activate cyclin-dependent kinases (Cdks) by dephosphorylating critical phospho-tyrosine and phospho-threonine residues on these proteins. Several types of studies indicate that Cdc25s can enhance cell proliferation and oncogenesis. Furthermore, overexpression of Cdc25A and/or B have been detected in several types of primary human cancers, including breast cancers. To further assess the oncogenic capacity of Cdc25B in vivo, we have generated transgenic mice that overexpress Cdc25B in the mammary epithelium, driven by the MMTV - LTR promoter. Although these mice are grossly normal for up to 18 months, the ectopic expression of Cdc25B in their mammary glands increases the susceptibility of these mice to induction of mammary tumors by the carcinogen 9,10-dimethyl-1, 2-benzanthracene (DMBA).
Insights
Overexpression of Cdc25B in mouse mammary glands increases susceptibility to carcinogen-induced breast cancer. This study highlights Cdc25B
Area of Science:
- Cell cycle regulation
- Oncogenesis
- Cancer biology
Background:
- Cdc25 phosphatases activate cyclin-dependent kinases (Cdks).
- Cdc25s promote cell proliferation and oncogenesis.
- Cdc25A and Cdc25B overexpression is detected in human cancers, including breast cancer.
Purpose of the Study:
- To assess the in vivo oncogenic capacity of Cdc25B.
- To investigate the role of Cdc25B in mammary tumor development.
Main Methods:
- Generated transgenic mice overexpressing Cdc25B in the mammary epithelium using the MMTV-LTR promoter.
- Administered the carcinogen 9,10-dimethyl-1,2-benzanthracene (DMBA) to induce mammary tumors.
Main Results:
- Transgenic mice overexpressing Cdc25B were grossly normal up to 18 months.
- Ectopic Cdc25B expression in mammary glands increased susceptibility to DMBA-induced mammary tumors.
Conclusions:
- Cdc25B overexpression enhances mammary gland susceptibility to chemical carcinogenesis.
- Cdc25B plays a role in promoting mammary oncogenesis in vivo.