Estradiol and fibulin‐1 inhibit motility of human ovarian‐ and breast‐cancer cells induced by fibronectin

Hayashido, Yasutaka; Lucas, Annick; Rougeot, Christian; Godyna, S; Argraves, W. Scott; Rochefort, Henri

doi:10.1002/(sici)1097-0215(19980209)75:4<654::aid-ijc26>3.3.co;2-k

Cited by 27 publications

(37 citation statements)

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“…More recent studies have demonstrated that estradiol significantly reduces invasiveness and that this inhibition is reversed by antiestrogens [83][84][85][86][87]. This conclusion was noted in several ER-positive cancer cell lines established from breast [83] or ovary [85], and in different ER-negative cancer cells constitutively expressing ER after stable transfection [45,84,87]. Similar results were also obtained on the migration of normal cells from vascular smooth muscle [86].…”

Section: Estrogens Inhibit Invasion Via Ere-regulated Genessupporting

confidence: 65%

“…The initial studies indicated that the invasiveness of MCF7 breast cancer cells was increased by antiestrogens [81,82]. More recent studies have demonstrated that estradiol significantly reduces invasiveness and that this inhibition is reversed by antiestrogens [83][84][85][86][87]. This conclusion was noted in several ER-positive cancer cell lines established from breast [83] or ovary [85], and in different ER-negative cancer cells constitutively expressing ER after stable transfection [45,84,87].…”

Section: Estrogens Inhibit Invasion Via Ere-regulated Genesmentioning

confidence: 96%

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Estrogens and their receptors in breast cancer progression: a dual role in cancer proliferation and invasion

Platet

Cathiard

Gleizes

et al. 2004

Critical Reviews in Oncology/Hematology

319

236

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Estrogens play an important role in regulating the growth and differentiation of normal, premalignant and malignant cell types, especially breast epithelial cells, through interaction with two nuclear estrogen receptors (ER and ERIn this review, we present a brief overview of the actions of estrogens in the different steps of breast carcinogenesis, including cancer progression to metastasis, and of their clinical consequences in the prevention, prognosis and treatment of the disease. The requirement of estrogen receptors, mainly of the alpha subtype, in normal mammary gland differentiation and growth has been evidenced by estrogen receptor deficiency in animals. The promotion of breast cancer carcinogenesis by prolonged exposure to estrogens is well-documented and this has logically led to the use of antiestrogens as potentially chemopreventive agents. In breast cancer progression, however, the exact roles of estrogen receptors have been less well established but they may possibly be dual. Estrogens are mitogenic in ER-positive cells and antiestrogens are an efficient adjuvant therapy for these tumors. On the other hand, the fact that estrogens and their receptors protect against cancer cell invasiveness through distinct mechanisms in experimental models may explain why the presence of ER is associated with well-differentiated and less invasive tumors.2

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Section: Estrogens Inhibit Invasion Via Ere-regulated Genessupporting

confidence: 65%

Section: Estrogens Inhibit Invasion Via Ere-regulated Genesmentioning

confidence: 96%

Estrogens and their receptors in breast cancer progression: a dual role in cancer proliferation and invasion

Platet

Cathiard

Gleizes

et al. 2004

Critical Reviews in Oncology/Hematology

319

236

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“…The biologic functions of these transcripts appear to be variant-specific (Moll et al, 2002). Fbln-1 can self-associate and bind to ECM proteins, including fibronectin, laminin and nidogen, and to the coagulation protein fibrinogen (Hayashido et al, 1998). Fbln-1 is found in basement membranes and in loose connective tissue associated with matrix fibres (Roark et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Immunological and pathobiological roles of fibulin-1 in breast cancer

et al. 2003

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Fibulin-1 (Fbln-1) is an immunogenic breast cancerrelated glycoprotein identified by serological analysis of cDNA expression library (SEREX) strategy. Here, we show that dendritic cells from two breast cancer patients elicited a CD4 þ -mediated T-cell response to Fbln-1 presentation. In both patients, an antibody response to Fbln-1 was also found. By contrast, a Fbln-1-seronegative patient and a weakly seropositive patient demonstrated no such T-cell response. Analysis of human breast cancers for Fbln-1 RNA and protein expression revealed the presence of Fbln-1C and -1D variants. Fbln-1 was detected in the cytoplasm and at the cell surface of different human breast carcinoma cell lines. Immunohistochemical analysis of 528 archival primary breast carcinomas showed the expression of Fbln-1 in 35% of the cases. When the immunohistochemical findings were compared against pathobiological information associated with each specimen, an inverse relationship between Fbln-1 and cathepsin D expression was observed (P ¼ 0.04). Furthermore, even though long-term survival was similar between Fbln-1-positive and -negative cases, the survival of Fbln-1-positive cases improved when a lymphoid infiltrate was present at the tumour site. Taken together, our findings of an Fbln-1-specific immunity and the improved survival associated with Fbln-1 expression in the presence of lymphoid infiltration point to a role of Fbln-1 in tumour immunosurveillance.

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“…We have recently shown that ®bulin-1 protein expression is increased in human ovarian epithelial cancers as compared to normal and benign tumors and that epithelial ovarian cells expressed ®bulin-1 mRNA in vivo . The ability of ®bulin-1 to bind extracellular matrix proteins such as ®bronectin and laminin and its localization at sites of epithelial mesenchymal transition suggest a role in cell attachment and motility (Hayashido et al, 1998;Pan et al, 1993;Balbona et al, 1992;Aspberg et al, 1999;Roark et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Estrogen induction and overexpression of fibulin-1C mRNA in ovarian cancer cells

Katsaros²,

et al. 2002

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Fibulin-1 is an extracellular matrix protein induced by estradiol in estrogen receptor (ER) positive ovarian cancer cell lines. Alternative splicing of ®bulin-1 mRNA results in four di erent variants named A, B, C and D that may have distinct biological functions. We studied the relative expression of ®bulin-1 mRNA variants and their estrogen regulation in human ovarian cancer cells. In ovarian tissues and cancer cell lines, ®bulin-1C and -1D are the predominant forms, whereas ®bulin-1A and -1B are weakly expressed. We developed a competitive PCR assay based on coampli®cation of ®bulin-1C and -1D to study the relative expression of these ®bulin-1 variants in human ovarian samples. In ovarian cancer cell lines and ovarian cancer samples, there was a marked increase in the ®bulin-1C:1D and ®bulin-1C:HPRT mRNA ratios as compared to normal ovaries. In the BG1 estrogen receptor positive ovarian cancer cell line, ®bulin-1C mRNA was induced by estradiol in a dose-and time-dependent manner. Since others and we have previously shown an increased expression of ERa as compared to ERb in ovarian cancer cells, we investigated whether ERa or ERb is involved in this induction. For this aim, MDA-MB-231 breast cancer cell line, which expresses both low basal levels of ERs and ®bulin-1, was infected with recombinant ERa or ERb encoding adenovirus and treated with estradiol. Fibulin-1C was induced by estradiol in ERa-but not ERb-infected cells, suggesting that ®bulin-1C induction is mediated through ERa. In ovarian tumors, a trend towards a correlation between ®bulin-1C and ERa expression levels was noted. In conclusion, this study showed an increased ®bulin-1C: -1D mRNA ratio in ovarian cancer cells as compared to normal ovaries. This ®nding suggests that the C variant may be involved in ovarian carcinogenesis. Fibulin-1C overexpression may thus be a clue for the understanding of a putative role of estrogens in ERa promoted ovarian tumor progression.

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Estradiol and fibulin‐1 inhibit motility of human ovarian‐ and breast‐cancer cells induced by fibronectin

Cited by 27 publications

References 0 publications

Estrogens and their receptors in breast cancer progression: a dual role in cancer proliferation and invasion

Estrogens and their receptors in breast cancer progression: a dual role in cancer proliferation and invasion

Immunological and pathobiological roles of fibulin-1 in breast cancer

Estrogen induction and overexpression of fibulin-1C mRNA in ovarian cancer cells

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