Fig. 5.
Fig. 5. Expression of dominant-negative STAT3 inhibits SCF-independent survival and proliferation mediated by D816H mutant c-Kit in MO7e cells. / (A) D816H mutant c-kit–transduced MO7e cells were subsequently transfected with the empty pcDNA3.1/Hygro(+) vector, vector containing the wild-type (WT) STAT3 (St3) or STAT1, and vector containing dominant-negative (YF) STAT3 or STAT1. SCF-independent survival was evaluated by counting the numbers of colonies grown in methylcellulose culture 3 weeks following transfection (see “Materials and methods”). The results are presented as mean ± SE from 3 independent experiments. (B) Clones were isolated from colonies in methylcellulose and cultured in suspension in the absence of SCF. SCF-independent proliferation was evaluated from 3 clones in each experimental group by counting the cell numbers over a period of 4 days. The results are presented as mean ± SE from 3 independent experiments.

Expression of dominant-negative STAT3 inhibits SCF-independent survival and proliferation mediated by D816H mutant c-Kit in MO7e cells.

(A) D816H mutant c-kit–transduced MO7e cells were subsequently transfected with the empty pcDNA3.1/Hygro(+) vector, vector containing the wild-type (WT) STAT3 (St3) or STAT1, and vector containing dominant-negative (YF) STAT3 or STAT1. SCF-independent survival was evaluated by counting the numbers of colonies grown in methylcellulose culture 3 weeks following transfection (see “Materials and methods”). The results are presented as mean ± SE from 3 independent experiments. (B) Clones were isolated from colonies in methylcellulose and cultured in suspension in the absence of SCF. SCF-independent proliferation was evaluated from 3 clones in each experimental group by counting the cell numbers over a period of 4 days. The results are presented as mean ± SE from 3 independent experiments.

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