| pubmed-article:9751635 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9751635 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
| pubmed-article:9751635 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:9751635 | lifeskim:mentions | umls-concept:C1512505 | lld:lifeskim |
| pubmed-article:9751635 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:9751635 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:9751635 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:9751635 | pubmed:dateCreated | 1998-10-1 | lld:pubmed |
| pubmed-article:9751635 | pubmed:abstractText | Interleukin-4 (IL-4) is a pleiotropic cytokine produced by mast cells and T lymphocytes that promotes proliferation and immunoglobulin class-switching in B cells. IL-4 receptors (IL-4Rs) are also expressed by nonhematopoietic cells as well as some tumor cells. Unlike its mitogenic effect on B cells, IL-4 inhibits the growth of some cancer cells in vitro. In this study, we show that IL-4R is expressed by breast and ovarian cancer cell lines. Furthermore, anchorage-dependent and -independent growth of breast cancer cell lines MCF-7 and MDA-MB-231 is inhibited by IL-4 treatment, and this effect requires IL-4R. Interestingly, IL-4 only inhibited proliferating breast cancer cells and had no effect on basal, unstimulated growth. We therefore characterized the effect of IL-4 on breast cancer cell growth stimulated by either estradiol or insulin-like growth factor I (IGF-I). In both anchorage-dependent and -independent growth assays, IL-4 inhibited estradiol-stimulated growth. The antiestrogen effect of IL-4 was not due to IL-4 interference with the estrogen receptor, because IL-4 did not interfere with estrogen receptor-mediated reporter gene transactivation. In contrast, IL-4 had no effect on IGF-I-stimulated proliferation. Because IGF-I is known to inhibit programmed cell death, we examined apoptosis as a possible mechanism of IL-4 action. We established that IL-4 induced apoptosis in breast cancer cells by five independent criteria: (a) morphological indicators including pyknotic nuclei and cytoplasmic condensation; (b) DNA fragmentation; (c) the formation of DNA laddering; (d) the cleavage of poly(ADP-ribose) polymerase; and (e) the presence of cells with sub-G1 DNA content. IL-4 increased the percentage of apoptotic cells in MCF-7 and MDA-MB-231 cells 6.0- and 6.7-fold over that of the control, respectively. Finally, the addition of IGF-I reversed IL-4-induced apoptosis, suggesting that the mechanism of IL-4-induced growth inhibition in human breast cancer cells is the induction of programmed cell death. | lld:pubmed |
| pubmed-article:9751635 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9751635 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9751635 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751635 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9751635 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:9751635 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:9751635 | pubmed:author | pubmed-author:YeeDD | lld:pubmed |
| pubmed-article:9751635 | pubmed:author | pubmed-author:LevA EAE | lld:pubmed |
| pubmed-article:9751635 | pubmed:author | pubmed-author:GoochJ LJL | lld:pubmed |
| pubmed-article:9751635 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9751635 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:9751635 | pubmed:volume | 58 | lld:pubmed |
| pubmed-article:9751635 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9751635 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9751635 | pubmed:pagination | 4199-205 | lld:pubmed |
| pubmed-article:9751635 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:9751635 | pubmed:meshHeading | pubmed-meshheading:9751635-... | lld:pubmed |
| pubmed-article:9751635 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9751635 | pubmed:articleTitle | Interleukin 4 inhibits growth and induces apoptosis in human breast cancer cells. | lld:pubmed |
| pubmed-article:9751635 | pubmed:affiliation | Department of Medicine, University of Texas Health Science Center, San Antonio 78284-7884, USA. | lld:pubmed |
| pubmed-article:9751635 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9751635 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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