Linked Life Data

12963983

Source:http://linkedlifedata.com/resource/pubmed/id/12963983

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-9-9
pubmed:abstractText
Malignant tumours contain zones of chronic or acute hypoxia, which influence their prognosis and progression. The goal of our study was to understand the role of hypoxia in radio-resistance in a squamous cell carcinoma cell line of the head and neck (KB-3-1 cells). Cell growth was evaluated by Trypan blue exclusion under chronic hypoxia (3-5% O2) for 4 weeks or under normal conditions (21% O2). Cells were then gamma-irradiated either by X-ray (2-6 Gy) or UV-C radiation (0.001-10 J/cm(2)). Apoptosis was estimated by double staining with orange acridine and ethydium bromide and fluorescence microscopy. DNA content was estimated by FACS analysis. Expression of Bax, Bcl-2 and P53 was assessed by immunofluorescence and Western blotting. ROS production was measured by dichlorofluorescein fluorescence. Cell growth depends on oxygen tension. It decreased by 42 and 70% at 5 and 3% O2 compared to control with a significant cell cycle arrest rather than increased mortality. Hypoxic cells are more radio-resistant (x2.5) than normoxic cells. Under chronic hypoxia, Bcl-2 increased considerably in cells compared to control, while Bax and P53 did not change. After irradiation, in hypoxic cells very weak expression of the pro-apoptotic Bax protein and no translocation of Bax to the mitochondria were observed. In addition, irradiation of control KB-3-1 cells demonstrated a large increase in ROS production (x2) compared to cells irradiated identically under hypoxia. In conclusion, chronic hypoxia: i) seems to slow-down cell growth of KB-3-1 cells without inducing apoptosis, ii) induces Bcl-2 overexpression and prevents radiation-induced apoptosis by inhibiting ROS production and altering Bax subcellular redistribution and conformational changes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1019-6439
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1033-41
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12963983-Anoxia, pubmed-meshheading:12963983-Apoptosis, pubmed-meshheading:12963983-Biological Transport, pubmed-meshheading:12963983-Blotting, Western, pubmed-meshheading:12963983-Cell Cycle, pubmed-meshheading:12963983-Cell Line, Tumor, pubmed-meshheading:12963983-Cell Survival, pubmed-meshheading:12963983-Coloring Agents, pubmed-meshheading:12963983-Dose-Response Relationship, Radiation, pubmed-meshheading:12963983-Gamma Rays, pubmed-meshheading:12963983-Humans, pubmed-meshheading:12963983-Microscopy, Fluorescence, pubmed-meshheading:12963983-Mitochondria, pubmed-meshheading:12963983-Oxygen, pubmed-meshheading:12963983-Protein Conformation, pubmed-meshheading:12963983-Proto-Oncogene Proteins, pubmed-meshheading:12963983-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:12963983-Reactive Oxygen Species, pubmed-meshheading:12963983-Time Factors, pubmed-meshheading:12963983-Trypan Blue, pubmed-meshheading:12963983-Ultraviolet Rays, pubmed-meshheading:12963983-Up-Regulation, pubmed-meshheading:12963983-X-Rays, pubmed-meshheading:12963983-bcl-2-Associated X Protein
pubmed:year
2003
pubmed:articleTitle
Chronic hypoxia protects against gamma-irradiation-induced apoptosis by inducing bcl-2 up-regulation and inhibiting mitochondrial translocation and conformational change of bax protein.
pubmed:affiliation
Fundamental and Applied Bioenergetics Laboratory, INSERM E02-21, Joseph Fourier University, BP 53X, 38041 Grenoble cedex 9, France. catherine.riva-lavieille@ujf-grenoble.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't