ZFIN Image: He et al., 2020, Figure 4

Image

Figure Caption

Figure 4 <styled-content toggle='no' style='fixed-case'>FST</styled-content> promoted leukemia growth by activating <styled-content toggle='no' style='fixed-case'>ERK</styled-content>

A

FST expression in different AML cell lines was detected by Western blotting.

B, C

FST317 and FST344 overexpression resulted in significant increases in FST transcription by RT–qPCR and protein by Western blot (B) and promoted ML‐2 cell growth in vitro (C). Green, ML‐2‐GFP; blue, ML‐2‐FST317; red, ML‐2‐FST344. The RT–qPCR experiments were performed in triplicates (B).

D, E

The clonogenicity of ML‐2 overexpressing GFP, FST317, and FST344 in vitro for 14 days. The CFU experiments were performed in triplicates (E).

F–H

The engraftment of ML‐2 (with luciferase gene) overexpressing GFP, FST317, and FST344 was quantified by bioluminescence imaging (F and G), and the survival of ML‐2‐engrafted NSG mice in vivo was recorded (H). Survival curve in panel H was analyzed by log‐rank test. *P < 0.05 and **P < 0.01.

I, J

RNA‐seq and RT–qPCR validation of upregulation of RET, IL2RA, and CCL5 after FST344 overexpression in ML‐2 cells. RT–qPCR experiments were performed in triplicates (J).

K, L

Overall survival analysis of patients from TCGA‐AML based on the differential expression of IL2RA and CCL5.

M

Activation of MAPK/ERK pathway in ML‐2 by FST344 overexpression was validated by Western blotting. Scale bar = 1 mm.

Data information: In (B, C, E, G, and J), data were presented as mean ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001 (Student's t‐test). ns: not significant.Source data are available online for this figure.

Acknowledgments

This image is the copyrighted work of the attributed author or publisher, and ZFIN has permission only to display this image to its users. Additional permissions should be obtained from the applicable author or publisher of the image. Full text @ EMBO Mol. Med.