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Hypoxia upregulates carcinoembryonic antigen expression in cancer cells
International journal of cancer, 2007-12, Vol.121 (11), p.2443-2450
Kokkonen, Nina
Ulibarri, Ines Fernandez
Kauppila, Annika
Luosujärvi, Hanne
Rivinoja, Antti
Pospiech, Helmut
Kellokumpu, Ilmo
Kellokumpu, Sakari
2007
Details
Autor(en) / Beteiligte
Kokkonen, Nina
Ulibarri, Ines Fernandez
Kauppila, Annika
Luosujärvi, Hanne
Rivinoja, Antti
Pospiech, Helmut
Kellokumpu, Ilmo
Kellokumpu, Sakari
Titel
Hypoxia upregulates carcinoembryonic antigen expression in cancer cells
Ist Teil von
International journal of cancer, 2007-12, Vol.121 (11), p.2443-2450
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2007
Link zum Volltext
Quelle
Wiley Blackwell Single Titles
Beschreibungen/Notizen
Carcinoembryonic antigen (CEA, ceacam5) is an important tumor‐associated antigen with reported roles, e.g., in immunological defense, cell adhesion, cell survival and metastasis. Its overexpression in cancer cells is known to involve transcriptional activation of the CEA gene, but the underlying molecular details remain unclear. Here, we show that hypoxia and intracellular alkalinization, 2 factors commonly found in solid tumors, increase CEA protein expression in breast (MCF‐7) and colorectal (CaCo‐2 and HT‐29) cancer cells. The increase was comparable (2–3‐fold) to that observed in colorectal carcinomas in vivo. CEA promoter analyses further revealed that this upregulation involves a known binding site for HIF‐1 transcription factor (5′‐ACGTG‐3′) within one of the CEA promoter's positive regulatory elements (the FP1 site; the E‐box). Accordingly, deletion or targeted mutagenesis of this motif rendered the CEA promoter unresponsive to hypoxia. Our chromatin immunoprecipitation data confirmed that endogenous HIF‐1α binds to the CEA promoter in hypoxic cells but not in normoxic cells. Moreover, overexpression of the hypoxia‐inducible factor (HIF‐1α) was sufficient to increase CEA protein expression in the cells. In contrast, c‐Myc, which is known to bind to the overlapping E‐box, did not potentiate HIF‐1α‐induced CEA expression. CEA overexpression in vivo was also found to coincide with the expression of carbonic anhydrase IX, a well‐known hypoxia marker. Collectively, these results define CEA as a hypoxia‐inducible protein and suggest an important role for the tumor microenvironmental factors in CEA overexpression during tumorigenesis. © 2007 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0020-7136
eISSN: 1097-0215
DOI: 10.1002/ijc.22965
Titel-ID: cdi_crossref_primary_10_1002_ijc_22965
Format
–
Schlagworte
Biological and medical sciences
,
Blotting, Western
,
Breast Neoplasms - metabolism
,
Caco-2 Cells
,
Carcinoembryonic Antigen - genetics
,
Carcinoembryonic Antigen - metabolism
,
carcinoembryonic antigen expression
,
Cell Hypoxia
,
Cell Line, Tumor
,
Chromatin Immunoprecipitation
,
Colorectal Neoplasms - metabolism
,
DNA-Binding Proteins - metabolism
,
Electrophoresis, Polyacrylamide Gel
,
Female
,
Fluorescent Antibody Technique, Indirect
,
Gastroenterology. Liver. Pancreas. Abdomen
,
Gene Expression Regulation, Neoplastic
,
HeLa Cells
,
Humans
,
hypoxia
,
Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
,
Male
,
Medical sciences
,
neoplasia
,
pH homeostasis
,
Polymerase Chain Reaction
,
Promoter Regions, Genetic
,
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
,
Transcription Factors - metabolism
,
Transcription, Genetic
,
Transfection
,
Tumors
,
Up-Regulation
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