Fig. 5

Depletion of ATF6 blocks proliferation of LNCaP cells and growth of xenograft tumors. (A) IF staining of ATF6 (green) and giantin (Golgi, red) in LNCaP cells treated with control or ATF6α siRNAs; bars, 10 μm. (B) ATF6, PSA, and AR W-B of the lysate of LNCaP cells transfected with control or ATF6 siRNAs; β-actin is a loading control. (C) ATF6 and AR W-B of the nuclear fraction from: transfected with control siRNAs and empty pEGFP-N1 vector, transfected with ATF6 siRNAs and empty pEGFP-N1vector, and transfected with ATF6 siRNAs followed by pEGFP-ATF6 plasmid corresponding to the WT hATF6; lamin B1 is a loading control. (D) Representative images of colonies formed by control and ATF6 KD LNCaP cells as described in the Materials and Methods section; bars, 200 μm. (E and F) Quantification of the colonies’ lengths (the longest diameter) (E) and the number of colonies (F) in 30 randomly selected areas for control and ATF6 KD LNCaP cells. Data were collected from three independent experiments and expressed as a mean ± SD; ** P < 0.01, t test. (G) The xenograft tumors in nude mice inoculated with control and ATF6 KD LNCaP cells. (H) Representative tumor derived from Ctrl LNCaP cells. (I) The tumor growth is presented as a ratio of tumor weight (g)/number of days after injection. Data were collected from four control and four ATF6 KD xenograft tumors and expressed as medians (min – max); ** P < 0.01, t test