PMID- 15304978
OWN - NLM
STAT- MEDLINE
DCOM- 20041026
LR  - 20191210
IS  - 0449-3060 (Print)
IS  - 0449-3060 (Linking)
VI  - 45
IP  - 2
DP  - 2004 Jun
TI  - Influences of the p53 status on hypoxia-induced gene expression.
PG  - 333-9
AB  - The p53 tumor-suppressor gene is one of the most frequently mutated genes in 
      human cancers, and its genetic alterations may play critical roles in 
      oncogenesis, tumor progression, and angiogenesis. To clarify the influence of the 
      p53 status on hypoxia-inducible gene expression, we first performed transfection 
      assays with a hypoxia-responsive vector carrying 5 hypoxia-responsive elements 
      upstream of the human CMV minimal promoter driving transcription of the 
      luciferase gene in various human tumor cell lines with wild-type (wt) or mutant 
      (mut) p53. As a result, hypoxia responsiveness considerably varied between cell 
      lines, and we could not obtain clear evidence that the hypoxia-inducible factor-1 
      (HIF-1) mediated gene expression in the wt-p53 cells was lower than that in cells 
      with mut-p53. It is interesting that SaOS2 cells (p53 null) showed the highest 
      luciferase activities under both aerobic and hypoxic conditions among tested 
      cells. Next, to elucidate the effects of endogenous wt- and mut-p53s, a 
      transfection assay and Northern blot analysis for VEGF transcription under 
      hypoxia were performed by using isogenic variants of HT1080 cells differing in 
      their p53 status. The luciferase and the endogenous VEGF mRNA expression were 
      apparently lower in a variant carrying mutations in both p53 alleles than in a 
      parental line harboring wt-p53, implying that some types of mutant p53 
      constitutively accumulated in cells can decrease both the basal and the 
      hypoxia-induced expressions in addition to wt-p53.
FAU - Liu, Junye
AU  - Liu J
AD  - Department of Therapeutic Radiology and Oncology, Kyoto University Graduate 
      School of Medicine.
FAU - Shibata, Toru
AU  - Shibata T
FAU - Qu, Runjiang
AU  - Qu R
FAU - Ogura, Masakazu
AU  - Ogura M
FAU - Hiraoka, Masahiro
AU  - Hiraoka M
LA  - eng
PT  - Comparative Study
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Radiat Res
JT  - Journal of radiation research
JID - 0376611
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (Vascular Endothelial Growth Factor A)
SB  - IM
MH  - *Cell Hypoxia
MH  - Cell Line, Tumor
MH  - Gene Expression Regulation, Neoplastic/*genetics
MH  - Humans
MH  - Mutagenesis, Site-Directed
MH  - Neoplasms/*genetics/*metabolism
MH  - Recombinant Proteins/*metabolism
MH  - Structure-Activity Relationship
MH  - Transcriptional Activation/genetics
MH  - Tumor Suppressor Protein p53/*genetics/*metabolism
MH  - Vascular Endothelial Growth Factor A/metabolism
EDAT- 2004/08/12 05:00
MHDA- 2004/10/27 09:00
CRDT- 2004/08/12 05:00
PHST- 2004/08/12 05:00 [pubmed]
PHST- 2004/10/27 09:00 [medline]
PHST- 2004/08/12 05:00 [entrez]
AID - JST.JSTAGE/jrr/45.333 [pii]
AID - 10.1269/jrr.45.333 [doi]
PST - ppublish
SO  - J Radiat Res. 2004 Jun;45(2):333-9. doi: 10.1269/jrr.45.333.