Five newly established oesophageal carcinoma cell lines: phenotypic and immunological characterization

Rockett, John C.; Larkin, Karilyn; Darnton, S. Jane; Morris, Alan; Matthews, H R

doi:10.1038/bjc.1997.42

Cited by 105 publications

(97 citation statements)

References 15 publications

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“…27 Chinese hamster ovary (CHO) cells stably transfected with human full length CAR cDNA (CHO-CAR; a kind gift of Dr J Bergelson, Division of Infectious Diseases, Children's Hospital of Philadelphia, Philadelphia, PA) and parental CHO cells were cultured in Ham's F12 medium containing 10% FCS. To permanently inhibit CAR expression a CAR-specific siRNA: CCAA GUACCAAGUGAAGACdTdT and a scrambled siRNA control: CACAAAAGUAUCGCGCAAGdTdT were cloned into the 'pSuper' vector system according to a standard protocol (Oligoengine, Seattle, WA) and transfected into OE19 and OE33 cells using Effectene (Quiagen, Hilden, Germany).…”

Section: Construction Of Tissue Microarrays and Immunohistological Inmentioning

confidence: 99%

Expression and function of the coxsackie and adenovirus receptor in Barrett's esophagus and associated neoplasia

et al. 2009

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Cell surface presence of the coxsackie and adenovirus receptor (CAR) is considered a crucial prerequisite for the uptake of attenuated adenovirus. In cancers, however, a frequent loss of CAR has been noted potentially hampering the success of adenovirus-based therapy. In esophageal Barrett's carcinomas and its precursor lesions CAR presence has not been systematically determined yet. Immunohistochemical assessment in tissue specimens of 111 patients revealed CAR-positivity in all cases of Barrett's esophagus, including various degrees of intraepithelial neoplasia. In contrast, no considerable CAR presence was seen in squamous esophageal epithelium. Among Barrett's carcinomas, 93% displayed CAR presence, whereas CAR-negativity was observed preferentially in advanced cancers. Aiming to evaluate whether this loss of CAR impacts tumor-biologic properties of esophageal adenocarcinomas we studied cell lines OE19 and OE33 and observed an increased proliferation, migration and invasion upon siRNA-mediated functional CAR knock down. In conclusion, our results indicate that CAR may provide a valuable target for adenovirus-based therapy of Barrett's carcinomas and its precursor lesions. These data do also suggest that CAR does not contribute substantially to carcinogenesis in Barrett's esophagus, however, it may be speculated that loss of CAR promotes tumor progression in advanced stages of Barrett's carcinomas.

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Section: Construction Of Tissue Microarrays and Immunohistological Inmentioning

confidence: 99%

Expression and function of the coxsackie and adenovirus receptor in Barrett's esophagus and associated neoplasia

et al. 2009

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“…A recent report revealed that SEG-1 cells are actually H460 lung adenocarcinoma cells (13). The H460 cells used in this study were reassessed by Winand Dinjens, Erasmus Medical Center, Rotterdam, the Netherlands using the Powerplex 16 TM system (Promega Corp., Madison, WI) to characterize 16 short tandem repeat markers. The resultant data matched for all 16 markers of H460 cells (supplemental data S1).…”

Section: Methodsmentioning

confidence: 99%

The Human Adenocarcinoma-associated Gene, AGR2, Induces Expression of Amphiregulin through Hippo Pathway Co-activator YAP1 Activation

Dong¹,

Gupta²,

Pai³

et al. 2011

Journal of Biological Chemistry

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Anterior Gradient Homolog 2 (AGR2) is expressed by the normal intestine and by most human adenocarcinomas, including those derived from the esophagus, pancreas, lung, breast, ovary, and prostate. Xenografts of human adenocarcinoma cell lines in nude mice previously demonstrated that AGR2 supports tumor growth. In addition, AGR2 is able to induce in vitro a transformed phenotype in fibroblast and epithelial cell lines. The mechanism underlying the growth promoting effects of AGR2 is unknown. The present study shows that AGR2 induces expression of amphiregulin (AREG), a growth promoting EGFR ligand. Induced AREG expression in adenocarcinoma cells is able to rescue the transformed phenotype that is lost when AGR2 expression is reduced. Additional experiments demonstrate that AGR2 induction of AREG is mediated by activation of the Hippo signaling pathway co-activator, YAP1. Thus AGR2 promotes growth by regulating the Hippo and EGF receptor signaling pathways. Anterior Gradient Homolog 2 (AGR2)2 encodes a 17 kDa protein that is highly conserved in vertebrates. AGR2 was first described in Xenopus laevis, where its expression is responsible for the development of a glandular organ called the cement gland (1). A significant role in tissue regeneration was established for AGR2 in salamanders where it functions in nerve-dependent limb regeneration (2). AGR2 is also expressed by secretory cells in the normal murine intestine (3). In humans, enhanced AGR2 expression was first described in breast cancer, which was followed by similar observations in most human adenocarcinomas, including those derived from the esophagus, pancreas, lung, ovary, and prostate (4 -11). Both in vitro and in vivo studies demonstrated that AGR2 promotes tumor growth and metastasis (3,6,12). In adenocarcinoma cell lines and nontransformed fibroblasts, AGR2 induces cell proliferation and anchorage-independent growth in soft agar. Human adenocarcinoma cell lines grown in vivo as mouse xenografts result in smaller tumors when AGR2 expression is reduced (3, 6). In vitro studies examining cell migration suggested that AGR2 may function in a non-cell autonomous fashion (3).The mechanisms responsible for AGR2 effects on growth and transformation are unknown. AGR2 expression in humans is restricted to epithelial cells, for which the EGF signaling pathway serves a regulatory role in controlling cell growth. The present study tested the hypothesis that AGR2 affects cell signaling, and potentially that of the EGFR pathway, which has established significance in epithelial cancers. EXPERIMENTAL PROCEDURESCell Lines-H460 lung adenocarcinoma cells obtained from Dr. David Beer (University of Michigan, Ann Arbor, MI) were previously known as SEG-1 and was the focus of a previous publication (3). A recent report revealed that SEG-1 cells are actually H460 lung adenocarcinoma cells (13). The H460 cells used in this study were reassessed by Winand Dinjens, Erasmus Medical Center, Rotterdam, the Netherlands using the Powerplex 16 TM system (Promega Corp., Madison, WI) to...

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“…Cell lines OE21(E) purified for epithelial phenotype, parent cell line derived from moderately differentiated oesophageal squamous cancer OE21 (Rockett et al, 1997), TE1 and TE2 (both moderately differentiated oesophageal squamous cancer, Nishihira et al, 1993), OE33(E) purified for epithelial phenotype, parent cell line derived from moderately well differentiated oesophageal adenocarcinoma OE33 (Rockett et al, 1997), Caco-2 (well differentiated adenocarcinoma colonic cell line) and SW-480 (poorly differentiated colonic cell line) were all routinely maintained in Dulbecco's modified eagle's medium with 10% calf serum supplemented with 100 u/ml pencillin and 0.1 mg/ml streptomycin. A dose response curve for the biological effect of TNF-a on epithelial cells was performed and 50 ng/ml was identified as the optimal dose for stimulation experiments (Perry et al, 1999).…”

Section: Cell Culturementioning

confidence: 99%

Tumour necrosis factor-α in Barrett's oesophagus: a potential novel mechanism of action

et al. 2002

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Barrett's metaplasia (BM) is an early lesion in the progression from oesophageal inflammation through dysplasia to the development of Barrett's adenocarcinoma (BA). Previous work indicates that BM and BA are associated with reduced E-cadherin expression and increased cytoplasmic/nuclear pools of its associated protein b-catenin. b-catenin participates in Wnt signalling and activates oncogene transcription by complexing with T-cells factors (TCF). One such oncogene is c-myc. We have previously shown that TNF-a can downregulate E-cadherin expression. Here, we assess TNF-a expression in Barrett's metaplasia and examine if TNF-a can promote b-catenin mediated transcription of oncogenes in a gastrointestinal model system. Employing immunohistochemistry and Western blot analysis of oesophageal tissue, epithelial expression of TNF-a increases with progression along the metaplasia -dysplasia -carcinoma sequence (P50.001). b-catenin mediated transcription was then assessed in TNF-a stimulated cell lines using the TOPFLASH reporter system whilst cmyc expression was assessed by real time PCR. In a columnar intestinal cell model, TNF-a induces c-myc expression which is induced via b-catenin mediated transcription (P50.05). This b-catenin mediated transcription is independent of NF-kB activation. Thus, TNF-a is up-regulated in the progression of Barrett's oesophagus and b-catenin mediated transcription of cmyc is a novel pathway whereby elevated levels of TNF-a may lead to oncogene transcription and altered biology in gastrointestinal epithelia and metaplasia.

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Five newly established oesophageal carcinoma cell lines: phenotypic and immunological characterization

Cited by 105 publications

References 15 publications

Expression and function of the coxsackie and adenovirus receptor in Barrett's esophagus and associated neoplasia

Expression and function of the coxsackie and adenovirus receptor in Barrett's esophagus and associated neoplasia

The Human Adenocarcinoma-associated Gene, AGR2, Induces Expression of Amphiregulin through Hippo Pathway Co-activator YAP1 Activation

Tumour necrosis factor-α in Barrett's oesophagus: a potential novel mechanism of action

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