Abstract:
:A stable cyclized 9-mer peptide (cP) containing the active site of alpha-alpha fetoprotein (alphaFP) has been shown to be effective for prevention of estrogen-stimulated tumor cell proliferation in culture or of xenographt growth in immunodeficient mice. cP does not block 17beta-estradiol (E2) binding to its receptors, but rather appears to interfere with intracellular processing of the signal that supports growth. To obtain insight on that mechanism we studied the effect of cP on the proliferation of MCF-7 cells in culture. Proliferation in the presence of 2 microM E2 is decreased up to 40% upon addition of 2 microg ml(-1) cP to the medium; the presence of cP did not increase cell death, cP reduced also the proliferation of estrogen-dependent ZR75-1 cells but had no effect on autonomous MDA-MB-231 cells, cP did not modify the number of binding sites for labeled E2 or affected cell death. We detected increased nuclear p21Cip1 immunoreactivity after cP treatment. Our results suggest that cP acts via p21Cip1 to slow the process of MCF-7 cells through the cycle.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
Sierralta WD,Epuñan MJ,Reyes JM,Valladares LE,Pino AMdoi
10.1007/978-0-387-69080-3_45subject
Has Abstractpub_date
2008-01-01 00:00:00pages
463-8eissn
0065-2598issn
2214-8019journal_volume
617pub_type
杂志文章abstract::It is well established that muscle fatigue, defined as a decline in maximal force generating capacity, is a common response to muscular activity. To what extent metabolic factors contribute to the reduced muscle function is still debated. Metabolic effects can affect muscle through different processes, either through ...
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