Establishment and characterisation of cell lines from patients with lung cancer (predominantly small cell carcinoma)

Baillie-Johnson, Hugo; Twentyman, Peter R.; Fox, Norma E.; Walls, G A; Workman, Paul; Watson, James V.; Johnson, Neil; Reeve, Julie G.; Bleehen, Norman M.

doi:10.1038/bjc.1985.220

Cited by 74 publications

(19 citation statements)

References 22 publications

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“…All these cell lines were derived from patients with pathologically confirmed SCLC (Pettengill et al 1980, Baillie-Johnson et al 1985. All SCLC cell lines were cultured in RPMI-1640 medium (Invitrogen) supplemented with 10% FCS and 10 mM HEPES, as described previously (Ray et al 1994).…”

Section: Methodsmentioning

confidence: 99%

Glucocorticoid receptor-mediated apoptosis in small-cell lung cancer requires interaction with BCL2

Schlossmacher¹,

Platt²,

Davies³

et al. 2013

Endocrine-Related Cancer

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Small-cell lung cancer (SCLC) tumours are highly aggressive. At the time of diagnosis, patients have often developed metastases, and overall prognosis is particularly poor, making effective treatment difficult. Novel mechanisms need to be identified as treatment targets. We have previously found low levels of the glucocorticoid receptor (GR) in SCLC cell lines and demonstrated that over-expression of GR increases tumour cell death both in vitro and in vivo. We hypothesise that low levels of GR impair its inhibitory effect on BCL2 and thus provide a survival advantage to SCLC cell lines. The mechanism behind GR-induced apoptosis is currently unknown; therefore, pro-and anti-apoptotic genes were investigated for their role in GR-mediated apoptosis signalling. We found that over-expression of wtGR via retroviral transduction causes the DMS 79 SCLC cell line to undergo caspase-mediated apoptosis within 72 h. Neither BAD nor BCL2L11 (BIM) mRNA and protein levels were affected by GR restoration implying that GR does not trigger apoptosis in the SCLC cell lines by up-regulating these pro-apoptotic genes. The anti-apoptotic BCL2 gene was significantly overexpressed in six SCLC cell lines and the BCL2 inhibitor ABT-737 increased apoptosis in all three cell lines tested. GR interacted with BCL2 in DMS 153, DMS 79 and COR-L42 cell lines, suggesting that a protein interaction between GR and BCL2 could play a role in GR-induced apoptosis. A deeper understanding of the molecular mechanism for increasing GR expression in SCLC could provide novel treatment strategies in the future.

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Section: Methodsmentioning

confidence: 99%

Glucocorticoid receptor-mediated apoptosis in small-cell lung cancer requires interaction with BCL2

Schlossmacher¹,

Platt²,

Davies³

et al. 2013

Endocrine-Related Cancer

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“…D. Carney and A. Gazdar (National Cancer Institute, Navy Medical Oncology Branch, Bethesda, MD). The derivation and characterization of the SCLC cell lines COR-L88, COR-L32, COR-IA2, COR-L47, and COR-L51 and the large cell NSCLC cell line COR-L23 have been described previously (14). These, together with the squamous cell lung carcinoma cell line BEN and the lung adenocarcinoma cell line MOR, were obtained from Dr. P. R. Twentyman, and the squamous cell lung cancer cell line LUDLU-1 was kindly supplied by Dr. P. H. Rabbitts (both from the Clinical Oncology and Radiotherapeutics Unit, Medical Research Council Centre, Cambridge, United Kingdom).…”

Section: Methodsmentioning

confidence: 99%

Role for membrane and secreted insulin-like growth factor-binding protein-2 in the regulation of insulin-like growth factor action in lung tumors

Reeve

Morgan²,

Schwander³

et al. 1994

Lung Cancer

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The insulin-like growth factors (IGFs) have been implicated in the autocrine and/or paracrine growth of a number of tumor types, including lung tumors. Importantly, insulin-like growth factor-binding proteins (IGFBPs), which both enhance and inhibit the physiological and biological actions of the IGFs, have been shown to be secreted in vitro by a wide range of tumors. In particular, IGFBP-2 is frequently produced by human tumor cells, suggesting that this protein may be an

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“…The derivation and characterization of the SCLC COR-L42 cell line has been described elsewhere (Baillie-Johnson et al, 1985). Briefly, this cell line shows a deletion in the short arm of chromosome 3 (Ibson et al, 1987), contains high levels of neuron-specific enolase and creatinine kinase BB, a low level of L-dopa decarboxylase activity (Baillie-Johnson et al, 1985), and does not express the GRP gene (Cardona et al, 1991).…”

Section: Cell Linementioning

confidence: 99%

“…Briefly, this cell line shows a deletion in the short arm of chromosome 3 (Ibson et al, 1987), contains high levels of neuron-specific enolase and creatinine kinase BB, a low level of L-dopa decarboxylase activity (Baillie-Johnson et al, 1985), and does not express the GRP gene (Cardona et al, 1991). These properties are consistent with its classification as a variant SCLC (SCLC-V) cell line .…”

Section: Cell Linementioning

confidence: 99%

Characterization of ligand binding and processing by gastrin-releasing peptide receptors in a small-cell lung cancer cell line

Cardona

Bleehen

Reeve

1992

Biochemical Journal

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The ligand-binding properties of the gastrin-releasing peptide (GRP) receptor and the cellular processing of GRP have been studied in the small-cell lung cancer (SCLC) cell line COR-L42. Scatchard analysis of GRP receptor expression indicated a single class of high-affinity receptors (Kd 1.5 nM) and approx. 6700 receptors/cell. GRP bound to its receptor with a K1 of 2.4 nm. The bombesin-related peptides neuromedin B (NMB) and phyllolitorin also bound to GRP receptors with K, values of 22.7 and 59.1 nm respectively. Binding of 125I-GRP to COR-L42 cells increased rapidly at 37°C, achieved a maximum at 10 min and declined rapidly thereafter. At 4°C, maximum binding was achieved at 30 min and the subsequent decline in cell-associated radioactivity was slower than that seen at 37 'C. Acid/salt extraction, to separate surface-bound ligand from internalized GRP, indicated that after receptor binding 125I-GRP was rapidly internalized. To determine the pathway of 125I-GRP degradation, binding studies were carried out with the lysosomotropic agent chloroquine (5 mM), and with phosphoramidon (10,UM), an inhibitor of the membrane-bound enzyme (EC 3.4.24.11).Both agents markedly inhibited the degradation of GRP, indicating that this process involves a lysosomal pathway and a phosphoramidon-sensitive pathway, possibly involving the EC 3.4.24.11 enzyme. GRP receptor down-regulation was observed following a 10 min exposure to 100 nM-GRP. With longer pretreatment times the number of binding sites recovered to 80 % of control values. Treatment with S mM-chloroquine plus GRP or cycloheximide (10,ig/ml) plus GRP demonstrated that the majority of GRP receptors are recycled. NMB and phyllolitorin pretreatment did not influence the subsequent binding of 125I-GRP, suggesting that these peptides do not down-regulate GRP receptors.

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Establishment and characterisation of cell lines from patients with lung cancer (predominantly small cell carcinoma)

Cited by 74 publications

References 22 publications

Glucocorticoid receptor-mediated apoptosis in small-cell lung cancer requires interaction with BCL2

Glucocorticoid receptor-mediated apoptosis in small-cell lung cancer requires interaction with BCL2

Role for membrane and secreted insulin-like growth factor-binding protein-2 in the regulation of insulin-like growth factor action in lung tumors

Characterization of ligand binding and processing by gastrin-releasing peptide receptors in a small-cell lung cancer cell line

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