Figure 7.

TAPIR knockdowns in radiation-resistant prostate cancer cells (LNCaP-RR) results in a renewed sensitization to X-ray treatment. The radioresistant LNCaP cell subline was used to analyze the effect of TAPIR knockdown on proliferation (colony formation assay) after X-ray treatment. Cells were treated with siRNA targeting TAPIR-1 or TAPIR-2 and, after plating, exposed to increasing doses of X-ray. After 10 d, surviving clonogenic cells were analyzed by counting cells that were able to form a cell clone or rather a colony. The TAPIR knockdown significantly reduces the plating efficiency and proliferation of the cells (A). TAPIR-1 and -2 knockdown leads to a significantly increased sensitization to radiation (B). The knockdown of TAPIR-1 and -2 leads to a dysregulation of DNA damage response key regulators in LNCaP-RR and to a DNA damage independent activation of the p53-DREAM signaling pathway, measured using qRT-PCR (C). The knockdown was validated using qRT-PCR (D). Data are shown as means ± s.d. n = 3, significance to control (SCRL): p ≤ 0.05 (*), p ≤ 0.01 (**), p ≤ 0.001 (***); two-sided student-t test.