Figure 6
From: Stress-induced tunneling nanotubes support treatment adaptation in prostate cancer
AR variant protein is involved in stress-induced TNTs formation. (A) 22Rv1 cells were transfected with siAR-V7 followed with treatment with SS. *p < 0.001 compared to siScr. (B) AR-V7 was overexpressed in LNCaP cells and TNT formation was quantified after CSS, ENZA or SS treatments. *p < 0.001 compared to mock. (C) LNCaP cells were transfected with AR-V7-expressing plasmid and then treated with CSS or ENZA +/− LY294002 for 24 hours. *p < 0.001 compared to mock. (D) LNCaP cells were transfected with plasmids for mock vector or AR-V7, and 24 hours later cells were transfected with siScr or siEps8. Cells were then treated with ENZA for 24 hours and TNTs formation was quantified. *p < 0.001 compared to siScr. (E) After CLU or YB-1 silencing in LNCaP cells, AR-V7 plasmid was transfected into the cells, followed with ENZA treatment. *p < 0.001 compared to mock. (F) A schema illustrating how ARPI stress induction of CLU/YB-1/AR-V7, via PI3K/AKT modulates Eps8-facilitated TNT production and intercellular communication for cancer cell survival under metabolic and therapeutic stress. All data is presented as average +/− SD from 3 independent experiments.
