The Functional Characterization of Normal and Neoplastic Human Enterochromaffin Cells

Modlin, Irvin M.; Kidd, Mark; Pfragner, Roswitha; Eick, Geeta; Champaneria, Manish C.

doi:10.1210/jc.2006-0110

Cited by 95 publications

(151 citation statements)

References 29 publications

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“…31 FACS sorted cells (%2 3 10 4 cells/100 lL) were cultured in Ham F12 medium (Gibco, Gaithersburg, Md) supplemented with 10% fetal calf serum and antibiotics (100 U penicillin/mL 1 100 lg streptomycin/mL; Sigma-Aldrich, St. Louis, Mo) (2 3 10 4 cells/well 96-well collagen I-coated plates; Becton Dickinson, San Jose, Calif) in a humidified atmosphere at 378C in 5% carbon dioxide for 72 hours.…”

Section: Normal Ec Cellsmentioning

confidence: 99%

“…31,36 Cells were incubated at 378C with 5% carbon dioxide. Population doubling level (PDL) 37 25 to 30 was used for all experiments.…”

Section: Neoplastic Ec Cells (Krj-i Cell Line)mentioning

confidence: 99%

“…31,36 TGFb1 (Santa Cruz Biotechnology, Santa Cruz, Calif [hBA-112, sc-4561]) was added at concentrations ranging from 1 pM to 100 pM (n ¼ 8 wells for each concentration) 38 and cells were incubated for 72 hours. MTT was added (final concentration 0.5 mg/mL per well) and incubated for 3 hours (378C at 5% carbon dioxide), and the reaction stopped by adding acid-isopropanol, and the formazan dye solubilized.…”

Section: Proliferation Studiesmentioning

confidence: 99%

“…11 It has not been possible to address these mechanistic questions previously because to our knowledge no homogenous human EC cell preparations or cell lines existed until we developed the methodology to isolate and culture normal human small intestinal EC cells. 31 In addition, we have developed and characterized a rapidly growing, longterm, primary tumor-derived, human carcinoid cell line, KRJ-I. 31,32 This small intestinal EC cell-derived in vitro model is ideal to examine the TGFb1 pathway because the alternatives such as the BON pancreatic tumor cell line, 33 the COLO320DM colonic cell line, 34 or the GOT1 liver metastases-derived cell line 35 are either of a mixed cell origin or are derived from metastases.…”

mentioning

confidence: 99%

“…31 In addition, we have developed and characterized a rapidly growing, longterm, primary tumor-derived, human carcinoid cell line, KRJ-I. 31,32 This small intestinal EC cell-derived in vitro model is ideal to examine the TGFb1 pathway because the alternatives such as the BON pancreatic tumor cell line, 33 the COLO320DM colonic cell line, 34 or the GOT1 liver metastases-derived cell line 35 are either of a mixed cell origin or are derived from metastases. In this study, using preparations of homogenous human EC cells and the KRJ-I cell line, we examined the proliferative effects of TGFb1 and then delineated aspects of the TGFb1 signaling pathway alterations that characterize the EC cell neoplastic phenotype.…”

mentioning

confidence: 99%

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Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

Kidd

Modlin

Pfragner

et al. 2007

Cancer

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Objective To examine whether and to what extent the intracellular trafficking features of HLA–B*2705, which is associated with the development of spondylarthritis (SpA), differ from those of HLA–B*2709 and HLA–B*0702, which are not associated with SpA. Methods HeLa cells were transfected with complementary DNA encoding for HLA–B proteins fused to Renilla luciferase or yellow fluorescent protein. The subcellular distribution of properly folded and unfolded/misfolded HLA–B proteins was examined by flow cytometry and confocal microscopy of cells labeled with ME1 and HC‐10 antibodies, respectively. HLA–B/HLA–B interactions were monitored in endoplasmic reticulum (ER)– and plasma membrane–enriched subcellular fractions, by bioluminescence resonance energy transfer (BRET). Results All 3 HLA–B alleles displayed a similar distribution pattern (properly folded heavy chain at the cell surface, unfolded/misfolded proteins only in the cytoplasm). By means of BRET, we provided evidence that both HLA–B*2705 and HLA–B*2709 formed more oligomers in the ER and the plasma membrane than did HLA–B*0702. The propensity of HLA–B*2705 to form oligomers in the ER was partly attributable to residue Cys67 of the molecule. For all 3 alleles, increased expression of HLA–B proteins was associated with intracytoplasmic accumulation of unfolded/misfolded proteins and intracellular vesicles, probably corresponding to expanded ER–Golgi intermediate compartments, in which these proteins accumulated together with the stress sensor BiP. Conclusion Our results suggest that the difference in disease susceptibility conferred by HLA–B*2705 and HLA–B*2709 cannot be explained by their different propensity to form dimers or misfolded proteins, thus presumably implicating other, still unknown factors.

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Section: Normal Ec Cellsmentioning

confidence: 99%

“…31,36 Cells were incubated at 378C with 5% carbon dioxide. Population doubling level (PDL) 37 25 to 30 was used for all experiments.…”

Section: Neoplastic Ec Cells (Krj-i Cell Line)mentioning

confidence: 99%

Section: Proliferation Studiesmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

Kidd

Modlin

Pfragner

et al. 2007

Cancer

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Gastrointestinal hormones in the regulation of gut function in health and disease

Valle

2014

Gastrointestinal Anatomy and Physiology

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Neuroendocrine tumor epidemiology

Hauso

Gustafsson

Kidd

et al. 2008

Cancer

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BACKGROUND. The National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program has proven to be a significant resource in US neuroendocrine tumor (NET) epidemiology. Norway also holds a robust and detailed cancer registry: the Norwegian Registry of Cancer (NRC). METHODS. SEER NET data were compared with corresponding NRC data in the time period 1993 to 2004 to determine whether there are differences in NET epidemiology between Norway and the United States. RESULTS. The SEER and NRC reported 17,312 and 2030 NETs, respectively. The overall Caucasian SEER NET incidence was 4.44, compared with 3.24 in the NRC. In the SEER white subset, bronchopulmonary NETs were the most common (incidence = 1.42; 32% of all NETs), compared with small intestinal NETs in the NRC (0.81; 26%). A marked increase in SEER NET incidence (37%‐40%) was observed in the period 2000 to 2004, compared with 1993 to 1997; an even more pronounced increase (72%) was seen in the NRC. African Americans exhibited a remarkably high overall NET incidence of 6.50; furthermore, among African Americans, rectal NETs were most common (1.65; 27%). Small intestinal NET incidence was ∼30% higher in men compared with women in all populations. The highest 5‐year survival rates were for rectal NETs (74%‐88%) in both databases, whereas prostatic NETs had the worst outcome (0%‐23%). At diagnosis, NETs were localized in 27% to 46% of patients. CONCLUSIONS. NET incidence in the US Caucasian population and in Norway is similar, but considerably higher (∼50%) among African Americans. NETs have been regarded as indolent tumors; however, the 5‐year survival is only ∼55%. Cancer 2008. © 2008 American Cancer Society.

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The Functional Characterization of Normal and Neoplastic Human Enterochromaffin Cells

Abstract: These data support novel methodology to purify live human EC cells for functional characterization and transcriptome assessment, which will allow identification of new targets to control the secretion and proliferation of SI carcinoids.

Cited by 95 publications

References 29 publications

Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

Gastrointestinal hormones in the regulation of gut function in health and disease

Neuroendocrine tumor epidemiology

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