Epithelial Cell Cultures From Normal and Cancerous Human Tissues2

Owens, Robert B.; Smith, Helene S.; Nelson‐Rees, Walter A.; Springer, Erik

doi:10.1093/jnci/56.4.843

Cited by 168 publications

(69 citation statements)

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“…In addition, we observed growth inhibition of LNCaP following long-term NDF treatment, accompanied by morphological changes such as cell clustering, withdrawal of processes, and increased cell ± cell membrane contact. These alterations are consistent with the reversion to an epithelial phenotype (Owens et al, 1976). In order to test this possibility, NDF-stimulated LNCaP will be analysed for increased expression of epithelial-speci®c markers.…”

Section: Discussionmentioning

confidence: 87%

ErbB kinases and NDF signaling in human prostate cancer cells

et al. 1997

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Section: Discussionmentioning

confidence: 87%

ErbB kinases and NDF signaling in human prostate cancer cells

et al. 1997

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“…In this study, eight of the 12 cell lines were found to produce CA19-9, and several produced CEA or DUPAN-2 as well. The four remaining cell lines were characterised mainly by morphological analysis (Lieber et al, 1975;Yunis et al, 1977;Owens et al, 1979;Yamada et al, 1986;Ikeda et al, 1990), which suggested that they originated from pancreatic cancer.…”

Section: Discussionmentioning

confidence: 99%

Production of endothelin-1 and thrombomodulin by human pancreatic cancer cells

Oikawa¹,

Kushuhara²,

Ishikawa³

et al. 1994

Br J Cancer

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Summary Analysis of bioactive substances produced by cancer cells is one approach to understanding the biological features of human cancer. One of these bioactive substances is endothelin (ET)-1, a peptide with potent vasoconstrictive activity produced by vascular endothelial cells. We have previously reported the production of ET-1 by several types of human cancer, especially pancreatic cancer cells. To elucidate whether these cancer cells might share biological characteristics with vascular endothelial cells, we investigated the production of three ET isoforms in pancreatic cancer cells, using a specific radioimmunoassay. Further, we also investigated whether these cells produce thrombomodulin (TM), another product of endothelial cells functioning as a modulator of procoagulant activity. ET-1 was detected in 11 of 12 pancreatic cancer cell lines (92%) while ET-2 and ET-3 were detectable in only one cell line. Gel filtration analysis confirmed the presence of ET-1. Moreover, TM was detected in the cell lysates of 11 of the 12 cell lines (92%) and it was released into the culture medium in the majority (58%) of these cell lines. TM mRNA was also detected in these cells. In addition, TM was demonstrated immunocytochemically along the cell surface. These results suggest that pancreatic cancer cells share two characteristics with endothelial cells: the production of ET-1 and TM.

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“…FHs 74 Int human small intestinal epithelial cells 34 were purchased from ATCC (Manassas, VA) and maintained in Hybri-Care Medium ATCC 46-X supplemented with 30 ng/ml epidermal growth factor (Sigma-Aldrich) and 10% FBS. RIE-1 rat intestinal epithelial cells 35 were maintained in DMEM containing 2 mM L-glutamine, 4500 mg/L glucose and 10% FBS.…”

Section: Methodsmentioning

confidence: 99%

An obligatory role for neurotensin in high-fat-diet-induced obesity

Song

Zaytseva

et al. 2016

Nature

227

237

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Obesity and its associated comorbidities (e.g., diabetes mellitus and hepatic steatosis) contribute to approximately 2.5 million deaths annually1 and are among the most prevalent and challenging conditions confronting the medical profession2,3. Neurotensin (NT), a 13-amino acid peptide predominantly localized in specialized enteroendocrine (EE) cells of the small bowel4 and released by fat ingestion5, facilitates fatty acid (FA) translocation in rat intestine6, and stimulates growth of various cancers7; the effects of NT are mediated through three known NT receptors (NTR1, 2 and 3)8. Increased fasting plasma levels of pro-NT (a stable NT precursor fragment produced in equimolar amounts relative to NT) are associated with increased risk of diabetes, cardiovascular disease and mortality9; however, a role for NT as a causative factor in these diseases is unknown. Here, we show that NT-deficient mice demonstrate significantly reduced intestinal fat absorption and are protected from obesity, hepatic steatosis and insulin resistance associated with high fat consumption. We further demonstrate that NT attenuates the activation of AMP-activated protein kinase (AMPK) and stimulates FA absorption in mice and in cultured intestinal cells, and that this occurs through a mechanism involving NTR1 and NTR3/sortilin. Consistent with the findings in mice, expression of NT in Drosophila midgut EE cells results in increased lipid accumulation in the midgut, fat body, and oenocytes (specialized hepatocyte-like cells) and decreased AMPK activation. Remarkably, in humans, we show that both obese and insulin-resistant subjects have elevated plasma concentrations of pro-NT, and in longitudinal studies among non-obese subjects, high levels of pro-NT denote a doubling of the risk of developing obesity later in life. Our findings directly link NT with increased fat absorption and obesity and suggest that NT may provide a prognostic marker of future obesity and a potential target for prevention and treatment.

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Epithelial Cell Cultures From Normal and Cancerous Human Tissues2

Cited by 168 publications

References 0 publications

ErbB kinases and NDF signaling in human prostate cancer cells

ErbB kinases and NDF signaling in human prostate cancer cells

Production of endothelin-1 and thrombomodulin by human pancreatic cancer cells

An obligatory role for neurotensin in high-fat-diet-induced obesity

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