[The role of PTEN-FAK signaling pathway in metastasis and invasive ability of leukemia cells].
Zhonghua Xue Ye Xue Za Zhi
; 30(2): 115-20, 2009 Feb.
Article
en Zh
| MEDLINE
| ID: mdl-19563023
ABSTRACT
OBJECTIVE:
To investigate the effect of the wild type phosphatase and tensin homolog deleted on chromosome 10 (PTEN), a tumor-suppressor gene on the proliferation and apoptosis of human chronic myeloid leukemia (CML) cells line (K562) in vitro and explore the influence of PTEN-FAK signaling pathway on invasion and metastasis of leukemia cells.METHODS:
The recombinant Ad-PTEN gene containing green fluorescent protein gene (Ad-PTEN-GFP) or the empty vector (Ad-GFP) was transfected into K562 cells and fresh leukemia cells from CML patients in blast crisis. The growth of K562 cells was assayed by MTT assay; the apoptosis rate was assessed by flow cytometry (FCM). PTEN and FAK mRNA levels were detected by real-time fluorescent relative- quantification reverse transcriptional PCR (FQ-PCR) and its protein levels by Western blot. The metastasis and invasive ability was examined by transwell chamber assay.RESULTS:
The growth of K562 cells was suppressed markedly when Ad-PTEN-GFP was transfected into K562 cells at the 200 multiplicity of infection (MOI). The maximum growth inhibition rate was 35.2%. Transwell results showed the number of cells entered the lower chamber in Ad-GFP group was 9.1 fold more than that in Ad-PTEN-GFP group;The ability of metastasis and invasion of fresh leukemia cells was also suppressed after transfection with Ad-PTEN-GFP. FAK and p-FAK proteins were down-regulated by 0.72 and 0.16 fold lower after transfected with Ad-PTEN-GFP compared with Ad-GFP group.CONCLUSIONS:
PTEN gene might inhibit the proliferation, metastasis and invasive ability of leukemia cells via down-regulating FAK expression.
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Base de datos:
MEDLINE
Asunto principal:
Infiltración Leucémica
/
Apoptosis
/
Proliferación Celular
/
Fosfohidrolasa PTEN
/
Quinasa 1 de Adhesión Focal
Límite:
Humans
Idioma:
Zh
Revista:
Zhonghua Xue Ye Xue Za Zhi
Año:
2009
Tipo del documento:
Article
País de afiliación:
China