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. 2021 Aug 12;10(8):2073. doi: 10.3390/cells10082073

Figure 7.

Figure 7

CTX1 induced the upregulation Fas and FasL in HL-60 cells through p38 MAPK-mediated c-Jun and ATF-2 phosphorylation. Without specific indication, HL-60 cells were directly treated with 800 nM CTX1 for 4 h, or incubated with 10 μM SB202190 for 1 h and then treated with 800 nM CTX1 for 4 h. (A) Effect of CTX1 on Fas and FasL protein expression in HL-60 cells (* p < 0.05, CTX1-treated cells compared to untreated control cells). (B) Detecting the expression of Fas and FasL mRNAs using qRT-PCR (mean ± SD, * p < 0.05). (C) CTX1 treatment elicited increase in transcriptional activity of Fas promoter and FasL promoter in HL-60 cells (mean ± SD, * p < 0.05). After transfection with indicated promoter constructs for 24 h, the transfected cells were treated with 800 nM CTX1 for 4 h and then harvested for measuring luciferase activity (mean ± SD, * p < 0.05). (D) Effect of SB202190 on the expression of Fas, FasL, p-c-Jun, and p-ATF-2 in CTX1-treated HL-60 cells (* p < 0.05, SB202190/CTX1-treated cells compared to CTX1-treated cells). Depletion of (E) c-Jun and (F) ATF-2 reduced CTX1-induced Fas and FasL expression. HL-60 cells were transfected with 100 nM control siRNA, c-Jun siRNA, or ATF-2 siRNA, respectively. After 24 h post-transfection, the cells were treated with 800 nM CTX1 for 4 h (* p < 0.05, CTX1-treated c-Jun siRNA- or ATF-2 siRNA-transfected cells compared to CTX1-treated control siRNA-transfected cells). (G) Effect of SB202190 on the viability of CTX1-treated HL-60 cells (mean ± SD, * p < 0.05).