[Effects of PTK787 on cell proliferation and expression of fak mRNA in K562].
The aim of this study was to investigate the effects of tyrosine kinase inhibitor PTK787 on cell proliferation, cell cycle and the expression of fak mRNA of human chronic myeloid leukemia (CML) cell line K562, and to explore the mechanism of PTK787 against acute myeloid leukemia. The MTT method was used to detect the effects of PTK787 in various concentrations and at different time points on proliferation of K562 cells; the flow cytometry was used to determine the effects of PTK787 in different concentrations on cell cycle of K562 cells; the RT-PCR was used to assay the expression of fak mRNA in K562 cells treated with PTK787 for 48 hours. The results showed that along with increasing of the concentration and prolonging of time, the inhibitory rate of PTK787 on K562 proliferation was gradually enhanced. The comparison between various concentration groups at same time or comparison between various time groups in same concentration showed significant differences (p < 0.05), in which the effect of 320 micromol/L PTK787 on cells was strongest, while the continuous increase of PTK787 concentration or prolong of action time did not enhance the inhibitory rate on K562 proliferation. With increasing of drug concentration, the cell proportion in G(1) phase gradually increased, the cell proportion in S phase gradually decreased, the comparison between various groups revealed significant differences (p < 0.05), however the continuous increase of drug concentration from 160 micromol/L did not obviously change the cell proportion in phases of cell cycle. With increasing of drug concentration, the expression of fak mRNA in K562 cells gradually reduced with significant differences between various groups (p < 0.05), but with continuous increase of drug concentration from 160 micromol/L, the effect of PTK787 on the expression of fak mRNA in K562 cells also did not obviously change. It is concluded that the PTK787 shows effect of anti-leukemia cells through inhibiting transformation of the K562 cells from G(1) phase into S phase and decreasing the expression of fak mRNA in cells.
Di
Xiao-Hua
XH
Department of Paediatrics, Affiliated Hospital, Guangdong Medical College, Zhanjiang 524001, Guangdong Province, China.
Chen
Ri-Ling
RL
Liu
Xiao-Li
XL
Tian
Chuan
C
Guo
Ya-Nan
YN
D002453:Cell Cycle; D049109:Cell Proliferation / Q000187:drug effects*; D051417:Focal Adhesion Kinase 1 / Q000235:genetics*; D015973:Gene Expression Regulation, Leukemic; D006801:Humans; D020014:K562 Cells; D010793:Phthalazines / Q000494:pharmacology*; D011725:Pyridines / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics*
D010793:Phthalazines; D011725:Pyridines; D012333:RNA, Messenger; C404768:vatalanib; D051417:Focal Adhesion Kinase 1; C496050:PTK2 protein, human