| Down-regulation of Bax-interacting factor-1 in colorectal adenocarcinoma. | |
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MedLine Citation:
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PMID: 18833585 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Bax-interacting factor-1 (Bif-1) protein is a member of the endophilin B family that plays a critical role in apoptosis, autophagy, and mitochondrial morphology. Loss of Bif-1 suppresses programmed cell death and promotes tumorigenesis. The connection of Bif-1 to colorectal cancer remains to be evaluated. METHODS: To determine Bif-1 expression in human colorectal adenocarcinoma (CRC), the authors performed immunohistochemistry using stage-oriented cancer tissue microarrays containing 102 CRC samples of different stages and 38 samples of normal colorectal mucosa (NR). Formalin-fixed, paraffin-embedded core sections on the tissue array were immunostained using the avidin-biotin-peroxidase method and the anti-Bif-1 murine monoclonal antibody. Bif-1 staining was scored by 2 independent observers. To examine Bif-1 mRNA levels, the authors performed DNA microarray analysis of 205 CRC and 10 NR samples. RESULTS: Bif-1 expression was negative in 22.5% (23 of 102) of CRCs. Moderate to strong Bif-1 staining was identified in 36.3% (37 of 102) of the tumors, and weak staining was noted in 41.2% (42 of 102). Twenty-six of 38 (68.4%) NR samples exhibited moderate to strong Bif-1 immunoreactivity, and none of them was negative. In 12 (31.6%) cases NR demonstrated weak Bif-1 stain. The mean (median) scores for CRCs and NR differed significantly: 3.2 (3.0) and 5.2 (6.0), respectively (P = .0003). The percentage of cases with negative expression also differed significantly between NR and CRC (P = .002). Decreased Bif-1 expression in CRCs was confirmed at the mRNA level by microarray analysis. CONCLUSIONS: The authors report the down-regulation of Bif-1 during the transition from NR to CRC, a novel finding in agreement with the tumor suppressor function of Bif-1. |
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Authors:
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Domenico Coppola; Farah Khalil; Steven A Eschrich; David Boulware; Timothy Yeatman; Hong-Gang Wang |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Cancer Volume: 113 ISSN: 0008-543X ISO Abbreviation: Cancer Publication Date: 2008 Nov |
Date Detail:
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Created Date: 2008-11-10 Completed Date: 2008-12-23 Revised Date: 2010-12-07 |
Medline Journal Info:
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Nlm Unique ID: 0374236 Medline TA: Cancer Country: United States |
Other Details:
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Languages: eng Pagination: 2665-70 Citation Subset: AIM; IM |
Affiliation:
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Department of Anatomic Pathology, H. Lee Moffitt Cancer Center, Tampa, Florida 33612-9497, USA. Domenico.Coppola@moffitt.org |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptor Proteins, Signal Transducing
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genetics,
metabolism* Adenocarcinoma / genetics, metabolism* Adult Aged Aged, 80 and over Colorectal Neoplasms / genetics, metabolism* Down-Regulation Female Gene Expression Profiling Humans Immunohistochemistry Male Middle Aged Oligonucleotide Array Sequence Analysis RNA, Messenger / analysis Tissue Array Analysis |
| Grant Support | |
ID/Acronym/Agency:
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CA82197/CA/NCI NIH HHS; R01 CA082197-08/CA/NCI NIH HHS; R01 CA082197-09/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Adaptor Proteins, Signal Transducing; 0/RNA, Messenger; 0/SH3GLB1 protein, human |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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