AI Article Synopsis
- The study investigated how estradiol (E2) and a cyclized peptide (cP) affect the growth of canine mammary cancer cells, focusing on their interaction with estrogen receptors (ER) found in the cells.
- In ER-positive cells, estradiol enhanced cell growth and activity of certain signaling proteins, while cP counteracted these effects and also reduced the expression of the HER2 protein.
- The findings suggest that cP may serve as a promising new treatment option for canine mammary cancer, with similar responses seen in human breast cancer cells.
Article Abstract
The effects of estradiol (E2) and of an AFP-derived cyclized peptide (cP) on the proliferation of primary cultures of cancer cells isolated from spontaneous canine mammary tumors were studied. The cellular response to E2 and cP was related to the expression of estradiol receptor (isoforms alpha and beta). In ER-positive cells, 2 nM estradiol increased cell proliferation and the phosphorylation of ERK1/2; 2 microg/ml cP inhibited all these effects. Estradiol also increased HER2 immunoreactivity in ER-positive cells, an effect that was reverted to its basal values by cP. Estradiol stimulated in these cells the release of MMP2 and MMP9 and the shedding of HB-EGF, effects that the cP did not affect. ER-negative cells were refractory to estradiol or cP. All canine mammary tumor cells in culture responded to treatments analogously to human mammary cancer cells. Our results support the proposal of cP as a new, potentially effective therapeutic agent for the management of mammary cancer.
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| http://dx.doi.org/10.3892/or_00000367 | DOI Listing |
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