A new cell line (8701-BC) from primary ductal infiltrating carcinoma of human breast

Minafra, Salvatore; Morello, Vincenza; Glorioso, F; Fiura, A M La; Rm, Tomasino; Feo, Salvatore; McIntosh, David G.; Woolley, David

doi:10.1038/bjc.1989.248

Cited by 69 publications

(54 citation statements)

References 27 publications

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“…The breast cancer cell lines used in this study were (Minafra et al, 1989; derived from primary tumour). The cell lines were maintained at 370C in Dulbecco's modified Eagle's medium (DMEM) with 5% fetal calf serum (FCS) and added non-essential amino acids, glutamine (2 mM), penicillin (100 U ml-') and streptomycin (100 [tg ml-'); all reagents were from ICN-Flow (High Wycombe, UK).…”

Section: Materials and Methods Cell Lines And Culture Conditionsmentioning

confidence: 99%

Proteinase inhibitors reduce basement membrane degradation by human breast cancer cell lines

Stonelake

Jones²,

Neoptolemos³

et al. 1997

Br J Cancer

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SummaryThe relative importance of different proteinases, and their inhibition, in the breakdown of human endothelial basement membrane (BM) by MDA-MB-231 and MCF7ADR human breast cancer cell lines has been studied using 35S-labelled (Fidler, 1990). Basement membrane degradation (BMD) is brought about by extracellular proteinases, and there is currently interest in inhibitors of these enzymes as potential therapeutic agents. Possible candidates for the proteinases involved in breast cancer invasion are found in each of the four major classes of proteinases, i.e. aspartic, cysteine, serine and matrix metalloproteinases (MMPs).The aspartic proteinase cathepsin D, a lysosomal enzyme, is oversecreted by breast cancer cells in vitro and may be a major proteinase involved in BMD (Briozzo et al, 1988). This view is supported by in vivo experiments in which transfection of cathepsin D cDNA resulted in a higher frequency of metastases in mice (Garcia et al, 1990). Nevertheless, some workers have questioned whether this lysosomal enzyme, which is only active at acid pH, has a role in invasion under physiological conditions (Johnson et al, 1993).The cysteine proteinases, cathepsins B, L and H, are also lysosomal enzymes that are overexpressed in breast cancer (Vasishta et al, 1988;Gabrijelcic et al, 1992). Cathepsin B from normal human liver and from human breast carcinomas has been shown to degrade components of BM at neutral pH as well as at acid pH (Buck et al,

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Section: Materials and Methods Cell Lines And Culture Conditionsmentioning

confidence: 99%

Proteinase inhibitors reduce basement membrane degradation by human breast cancer cell lines

Stonelake

Jones²,

Neoptolemos³

et al. 1997

Br J Cancer

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“…A1 forms lytic lesions in bone after intracardiac injection into nude mice (unpublished data Z.B.). BC61, BC3A, and 8701 are clones derived from a parental cell line that came from a biopsy of a ductal infiltrating carcinoma of the breast [32,33]. Furthermore, these cells have been reported to express PTHrP and the PTHrP receptor [34,35].…”

Section: The Expression Of Pthrp Erbb Receptors and Egfr Ligands In mentioning

confidence: 99%

Amphiregulin-EGFR signaling regulates PTHrP gene expression in breast cancer cells

Gilmore

Scott

Bouizar

et al. 2007

Breast Cancer Res Treat

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Parathyroid hormone-related protein (PTHrP) is an autocrine/paracrine factor produced by breast cancer cells that is speculated to play a major role in permitting breast cancer cells to grow into the bone microenvironment by stimulating the bone resorption axis. It has been previously shown that EGFR signaling induces the production of PTHrP in several primary and transformed epithelial cell types. Therefore, we investigated the relationship between EGFR and PTHrP gene expression in human breast cancer cells. Of a panel of 7 breast epithelial and cancer cell lines, the osteolytic, EGFRpositive lines (MDA-MB-231 and NS2T2A1) exhibited higher levels of PTHrP transcript expression. Amphiregulin mRNA levels in all lines were approximately 2 orders of magnitude higher than those of TGFα or HBEGF. In the EGFR bearing lines, the receptor was phosphorylated at tyrosine 992 under basal conditions, and the addition of 100 nM amphiregulin did not lead to the phosphorylation of other tyrosine residues typically phosphorylated by the prototypical ligand EGF. Treatment of the EGFR positive lines with the EGFR inhibitor PD153035 and amphiregulin-neutralizing antibodies reduced PTHrP mRNA levels by 50-70%. Stable EGFR expression in the MCF7 line failed to increase basal PTHrP mRNA levels; however, treatment of this cell line with exogenous EGF or amphiregulin increased PTHrP transcription 3-fold. Transient transfection analysis suggests that the MAPK pathway and ETS transcription factors mediate EGFR coupling to PTHrP gene expression. Taken together, it appears that autocrine stimulation of EGFR signaling by amphiregulin is coupled to PTHrP gene expression via EGFR Tyr992 and MAPK, and that this pathway may contribute to PTHrP expression by breast tumor cells.

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“…The major aspects were the over-deposition of type V collagen normally expressed at very low levels in adult tissues, and the appearence an onco-foetal form of interstitial collagen (OF/LB) [17,18,19]. Biological assays performed with a neoplastic cell line (8701-BC), isolated from a primary DIC [20], demonstrated that different collagen substrates were able to promote distinct behaviors of the cell population: in particular, the onco-foetal collagen enhanced cell proliferation and migration and promoted invasivity both "in vitro" and "in vivo", whilst type V collagen exerted an antagonistic effect, restraining both cell growth and "in vitro" invasivity [2,8,21,22,23,24].…”

Section: Introductionmentioning

confidence: 99%

Type V collagen induces apoptosis of 8701-BC breast cancer cells and enhances m-calpain expression

et al. 2000

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IntroductionWe previously reported that ductal infiltrating carcinomas (DIC) of the human breast display profound modifications of the stromal architecture, associated with anomalous collagen composition. The major alterations observed in the interstitial collagen were an abnormal ratio between type I and type III collagens, the appearence of an onco-foetal form of collagen (OF/LB) and a relative increase of type V collagen content. Biological assays performed by culturing a DIC-derived cell line (8701-BC) onto type V collagen substrate demonstrated that the latter was able to restrain cell growth and to inhibit cell motility and invasion "in vitro", differently from what found with other collagen species tested. AimsTo search for molecular mechanisms underlying the observed inhibitory effect of collagen type V on breast cancer cells. As a reference model, we used culture substrates prepared with type IV collagen, which represents the physiological substrate for cells of epithelial origin. MethodsApoptosis was studied by both fluorescence microscopical analyses of cell viability and DNA fragmentation assays in preparations of 8701-BC cells grown onto either type V and type IV collagen. Differences in gene expression following cell adhesion onto the two substrates were analyzed by a "differential display" PCR (DD-PCR) technique and Western blot. ResultsIn this paper we demonstrate that the inhibitory effect exerted by type V collagen is consistently associated with the switching-on of a death program by a significant proportion of the cell culture, concomitant with the formation of cohesive cell islands displaying a progressive decrease of cell spreading. DD-PCR and Western blot assays demonstrated a consistent association of type V collagen-promoted apoptosis with the up-regulation of the large subunit of m-calpain (L-mC) at both mRNA and protein level. Cell exposure to calpain inibitor I decreased the amount of DNA fragmentation by 30%. DiscussionThe present data substantiate our previous postulates that in cases of breast DIC the zonal increase of type V collagen contribute to the assembly of a "non-permissive" micro-environment for tumor cells, antagonist to other local permissive substrates. It is therefore conceivable that the spatiotemporal derangement of stromal components may actively modulate neoplastic cell behavior and metastatic propensity, thus contributing to the selection and development of more or less malignant tumor phenotypes. Keywords apoptosis, breast cancer, calpain, collagen type V, differential display.

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A new cell line (8701-BC) from primary ductal infiltrating carcinoma of human breast

Cited by 69 publications

References 27 publications

Proteinase inhibitors reduce basement membrane degradation by human breast cancer cell lines

Proteinase inhibitors reduce basement membrane degradation by human breast cancer cell lines

Amphiregulin-EGFR signaling regulates PTHrP gene expression in breast cancer cells

Type V collagen induces apoptosis of 8701-BC breast cancer cells and enhances m-calpain expression

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