Fig. 4

ATF3 suppresses PTK2 expression in PCa cells (a) RNA-Sequencing shows the ATF3 and PTK expression with reverse tendency under ASC-J9®^. treatment in C4–2 cells. b The linear regression shows ATF3 and PTK2 with negative correlation based on GEO Database GDS1239. c PTK2 mRNA expression in three human prostate databases (GDS2545, GDS1439, and GDS3289) demonstrate late stage tumors have higher PTK2 expression. d IHC from clinical samples show PTK2 expression lower in ADPC (early stage) and higher in CRPC (late stage) tumors. e Overexpressed ATF3 (oeATF3) could suppress PTK2 expression in C4–2 (left) and CWR22Rv1 (right) cells. f qRT-PCR revealed ASC-J9® treatment could decrease PTK2 expression in C4–2 (left) and CWR22rv1 (right) cells. g Western Blots show ASC-J9® treatment could suppress PTK2 expression level in C4–2 (left) and CWR22Rv1 (right) cells. h The diagram (upper left) shows ATF3 response element that is predicted by JASPAR (lower left) in the promoter of PTK2 and the ATF3 response element. Chip-PCR (upper right) and Chip-qRT-PCR (lower right) show ATF3 can bind to PTK2’s promoter region in C4–2 cells. i Luciferase assays show ASC-J9® could suppress PTK2 expression level and NAC could partially reverse this suppression in C4–2 cells. (J-K) MTT (j) and Invasion assays (k) show that oePTK2 can partly reverse the oeATF3 and ASC-J9® treatment effects in C4–2 (upper) and CWR22Rv1 (lower) cells. Data represent the mean ± SD except qRT-PCR represent the mean ± SEM. *p < 0.05, **p < 0.01, ns = not significant, by unpaired Student t test