Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2001-10-12
pubmed:abstractText
Recent studies indicate that wild-type p53 can trigger cell apoptosis induced by many chemotherapeutic agents which induce DNA damage or cause disruptions of DNA metabolism, such as ADM, 5-FU, VP-16 and radiation. We introduced the wild-type p53 gene into a MDR cell line KBV200 in which the endogenous p53 was found to be rearranged. By G418 selection and Northern blot analysis, a G418-resistant clone named KBV200-p53 was obtained which continuously expressed the exogenous wild-type p53 mRNA. After treatment with Vincristine(VCR), the wild type p53-expression cells presented typical morphology characteristic of apoptosis analysed under electron and fluorescence microscopes. Flow cytometer analysis showed that the KBV200-p53 cells were more readily undergo apoptosis than their parental cells KBV200. After treatment with VCR 600 nmol.L-1 for 24 h, the apoptotic percentage of KBV200-p53 and KBV200 cells was about 42.4% and 8.4%, respectively. This result indicates that wild-type p53 stimulates VCR-induced apoptosis in KBV200 cells.
pubmed:language
chi
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0513-4870
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
565-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
[Wild-type p53 stimulates vincristine-induced apoptosis].
pubmed:affiliation
Cancer Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021.
pubmed:publicationType
Journal Article, English Abstract, Research Support, Non-U.S. Gov't