ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    ISSN: 0730-2312
    Keywords: gene regulation ; stable transfection ; CAT assay ; sodium butyrate ; mRNA ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A number of studies suggest that an inverse correlation exists between the epidermal growth factor-receptor and the estrogen receptor expression in primary human breast carcinoma as well as in established human breast carcinoma cell lines. Recent studies suggest that the epidermal growth factor-receptor does not regulate the estrogen receptor gene expression. Whether the estrogen receptor regulates the epidermal growth factor-receptor gene expression is not known. We addressed this question by stably transfecting the estrogen receptor cDNA into the estrogen receptor-negative human breast carcinoma cell line MDA-MB-231. Constitutive expression of functional estrogen receptors in the transfactants resulted in increased mRNA levels of both epidermal growth factor-receptor and transforming growth factor α. Estradiol treatment of transfected cells, although enhancing transforming growth factor α mRNA levels, did not modulate epidermal growth factor-receptor mRNA levels. The estrogen receptor-transfected cells grown in estrogenic regular medium, however, exhibited lower constitutive levels of epidermal growth factor-receptor mRNA than in steroid-stripped medium, suggesting that estrogens coupled with some factors normally present in the regular medium may indeed downmodulate epidermal growth factor-receptor mRNA. Sodium butyrate treatment enhanced epidermal growth factor-receptor mRNA levels in nontransfected cells grown in regular estrogenic as well as in steroid stripped medium. Sodium butyrate enhancement of epidermal growth factor-receptor mRNA levels was completely abolished in estrogen receptor-transfected cells grown in regular estrogenic medium and blunted in steroid stripped medium. Using various epidermal growth factor-receptor gene promoter-CAT constructs in transient transfection assays, we further demonstrate that sodium butyrate enhanced transcription of the epidermal growth factor-receptor gene. The putative sodium butyrate responsive element(s) appears to localize within the proximal 384 bp of the epidermal growth factor-receptor gene promoter region. Although the interactions between estrogen receptor and epidermal growth factor-receptor are rather complex, taken together, our data suggest that estrogen receptor can indeed modulate the epidermal growth factor-receptor mRNA expression.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 0730-2312
    Keywords: genistein ; breast cancer ; p21WAF1/CIP1 ; G2/M arrest ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Genistein has been proposed to be responsible for lowering the rate of breast cancer in Asian women but the mechanism for this chemopreventive effect in vivo is unknown. In this study, we present in vitro evidence that genistein inhibits cell proliferation similarly in ER-positive and ER-negative human breast carcinoma cell lines. This inhibition is associated with specific G2/M arrest and induction of p21WAF1/CIP1 expression. Genistein results in a five- to six-fold increase in p21WAF1/CIP1 mRNA levels and a three- to four-fold increase in protein levels, only a 1.5-fold increase in p21WAF1/CIP1 transcription but a three- to six-fold increase in p21WAF1/CIP1 mRNA stability. The increase in p21WAF1/CIP1 is followed by increased apoptosis. The similar effects of genistein on a number of breast carcinoma cell lines with different ER and p53 status suggest that the actions of genistein reported here are mediated through ER and p53 independent mechanisms. The chemopreventive effects of genistein in vivo could be mediated along an identical or similar anti-proliferative pathway. J. Cell. Biochem. 69:44-54, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 0730-2312
    Keywords: transfection ; CAT assays ; gene expression ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. The ER-negative cells inherently express lower levels of RARα and retinoic acid response element (RARE)-mediated RA-induced CAT activity. In this study we report that when ER-negative MDA-MB-231 cells were transfected with the ER gene they not only expressed higher levels of RARα and RARE-mediated RA-induced CAT gene expression, but their growth was now inhibited by RA. Estrogen enhanced RARα gene expression not only in established ER-positive cell lines but also in ER-transfected MDA-MB-231 cells. The estrogen effect appears to be direct and at the gene transcription level since it did not alter the stability of RARα mRNA and cycloheximide failed to block estrogen-mediated enhancement of RARα gene expression. Our data strongly suggest that ER-mediated enhancement of RARα levels plays an important role in RA inhibition of HBC growth. In addition, we also report here that HBC cells appear to express a unique isoform(s) of RARα which was detected only when the full-length RARα cDNA was used as a probe; the RARα1 and RARα2 specific probes failed to hybridize with the HBC specific RARα message.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Retinoids modulate cellular proliferation and mediate gene function through a series of nuclear receptors. The retinoic acid nuclear receptor β (RARβ) plays an important role in the differentiation of a number of cell types. We now demonstrate that RARβ expresion is confined to normal mammary tissue and is not expressed in either immortalized normal or malignant cell lines. Treatment of RARβ-transfected MDA-MB-231 cells with 1 μM all-trans-retinoic acid (RA) significantly inhibited monolayer growth of the cells which express recombinant RARβ. RARβ-expressing MDA-MB-231 cells formed significantly smaller and fewer colonies soft agar than the mock-transfected cells. Addition of 1 μM RA stimulated colony size and number in the RARβ-transfected MDA-MB-231 cells. In contast to the RARβ-expressing cells, colony formation by the RARβ-expressing cells was similar to the mock-transfected controls and the addition of 1 μM RA to the RARα-transfected cells inhibited colony formation. While demonstrating decreased colony formation in agar, RARβ-expressing MDA-MB-231 cells failed to exhibit decreased growth in SCID mice. Our results show that RARβ functions as a negative regulator of growth in breast epithelial cells. In addition, the growth of these cells is differentially regulated by RARα and RARβ which is most likely the result to the modulation of different genes. © 1995 Wiley-Liss Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Insulin-like growth-factors I and II (IGF-I, II) are potent mitogens for breast carcinoma proliferation. In extracellular fluids, most of the IGF-I and II is associated with specific IGF-binding proteins (IGFBPs). The role of these IGFBPs in IGF action is still not clear, but it has been demonstrated that these proteins may either enhance or inhibit IGF-mediated cellular effects. Synthesis and secretion of IGFBPs have been demonstrated in breast carcinoma cells. In this study, we examined retinoic acid (RA) and IGF-I modulation of IGFBP mRNA and IGFBP levels in two ER-negative human breast carcinoma cell lines. Treatment of MDAMB-231 and MDA-MB-468 cells with RA increased the levels in conditioned media of a Mr 42-46-kDa IGFBP, which was immunoprecipitated by an IGFBP-3 antibody. IGF-I also increased the accumulated levels of IGFBP-3 in the conditioned media of both cell lines. Both cell lines expressed high basal levels of IGFBP-3 mRNA; the addition of RA increased IGFBP-3 mRNA levels by 1.5-fold, whereas the addition of IGFI had no effect on IGFBP-3 mRNA levels in either cell line. The difference in the magnitude of the RA enhancement of IGFBP-3 mRNA levels (1.5-fold) and RA stimulation of IGFBP-3 levels in conditioned media (3.5-4-fold) suggests that some of the effect of RA is at a posttranscriptional level. IGF-I increased the levels of IGFBP-2 and IGFBP-5 in conditioned media by greater than tenfold but had no effect on IGFBP-2 and IGFBP-5 mRNA levels, again suggesting the involvement of posttranscriptional controls. Pretreatment of MDA-MB-468 and MDA-MB-231 cells with IGF-I receptor antibody (αIR3) blocked the IGF-I effect on IGFBP-3 levels in the media in both cell lines and IGFBP-2 and IGFBP-5 secreted levels in MDA-MB-468 cell conditioned media. The addition of RA also blocked IGF-I stimulation of IGFBP2 and IGFBP-5 levels. Cycloheximide treatment completely blocked the RA and/or IGF-I-mediated modulation of these binding proteins, suggesting that these agents enhance IGFBP-3, IGFBP-2, and IGFBP-5 synthesis and consequent secretion. MDA-MB-468 cells expressed IGFBP-5 mRNA, whereas both MDA-MB-231 and MDA-MB-468 expressed IGFBP-6 mRNA. RA enhanced IGFBP-6 gene expression by threefold in MDA-MB-231 cells, whereas IGF-1 had no effect on IGFBP-6 gene expression in either cell line. These results demonstrate that RA and IGF-I modulate IGFBP levels in a number of breast carcinoma cell lines. Such modulation of IGFBPs may in turn affect IGF mediated cellular responses and thus the biologic behavior of these malignant cells.
    Additional Material: 10 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The insulin-like growth factors (IGFs) are potent mitogens for malignant cell proliferation. The majority of secreted IGFs are bound to specific IGF-binding proteins (IGFBPs) that are secreted by a large number of cells. These proteins may either inhibit or enhance IGF actions. Breast carcinoma cells secrete a variety of IGFBPs. We have previously demonstrated that retinoic acid (RA) inhibition of IGF-l- stimulated MCF-7 cell proliferation is associated with increased IGFBP-3 levels in the conditioned media. We therefore investigated the effect of recombinant IGFBP-3 as well as IGFBP-2, -4 and -5 on IGF-l stimulation of DNA synthesis and IGF-I binding in the MCF-7 human breast carcinoma cell line. IGFBP-2 and -3 enhanced IGF-l stimulation of DNA synthesis in MCF-7 cells while IGFBP-4 and -5 had no effect. Transfection of MCF-7 cells with an IGFBP-3 expression vector resulted in the enhanced secretion of IGFBP-3 with an accompanying increase in IGF-l binding as well as increased cell proliferation upon treatment of the cells with IGF-l. IGF-l preincubation of MCF-7 cells transfected with control pSVneo plasmids results in cells refractory to further IGF-l stimulation of thymidine incorporation while IGF-l continues to stimulate [3H]-thymidine incorporation in IGFBP-3-transfected MCF-7 cells, suggesting that IGFBP-3 protects the cells from IGF-l-mediated down regulation of its receptor. Therefore, IGFBP-3 secreted by MCF-7 cells can enhance IGF-l stimulation of DNA synthesis, increase IGF-l binding to these cells, and prevent IGF-l-induced desensitization of its own receptor, suggesting that IGFBP-3 plays a significant role in IGF-l-mediated breast carcinoma proliferation. © 1994 Wiley-Liss, Inc.
    Additional Material: 10 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...