Figure 4
Figure 4. S1PR1 antagonist FTY720 induced apoptosis and growth inhibition of ABC-DLBCL tumor cells through abrogating S1PR1/STAT3 signaling. (A) FTY720 treatment inhibited ABC-DLBCL tumor cell proliferation. ABC-DLBCL cell lines, Ly3 and Ly10, were treated with FTY720 at different concentrations as indicated for 24 or 48 hours. The relative cell numbers of different treatments were determined by MTS assay. (B) Treating ABC-DLBCL tumor cells with FTY720 induced apoptosis. The percentage of viable cells was determined by flow cytometry to detect annexin V and propidium iodide (PI) double-negative cells. (C) FTY720 treatment inhibited STAT3 activity in ABC-DLBCL tumor cells. The levels of S1PR1 and phospho-STAT3 in Ly3 and Ly10 ABC-DLBCL cells after FTY720 treatment (6 hours) were determined by Western blot analysis. All data are representative of results from 3 independent experiments.

S1PR1 antagonist FTY720 induced apoptosis and growth inhibition of ABC-DLBCL tumor cells through abrogating S1PR1/STAT3 signaling. (A) FTY720 treatment inhibited ABC-DLBCL tumor cell proliferation. ABC-DLBCL cell lines, Ly3 and Ly10, were treated with FTY720 at different concentrations as indicated for 24 or 48 hours. The relative cell numbers of different treatments were determined by MTS assay. (B) Treating ABC-DLBCL tumor cells with FTY720 induced apoptosis. The percentage of viable cells was determined by flow cytometry to detect annexin V and propidium iodide (PI) double-negative cells. (C) FTY720 treatment inhibited STAT3 activity in ABC-DLBCL tumor cells. The levels of S1PR1 and phospho-STAT3 in Ly3 and Ly10 ABC-DLBCL cells after FTY720 treatment (6 hours) were determined by Western blot analysis. All data are representative of results from 3 independent experiments.

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