Calprotectin induces cell death in human prostate cancer cell (LNCaP) through survivin protein alteration.
Calprotectin (CP), an abundant heterodimeric cytosolic protein of neutrophils, conveys a variety of functions such as tumor cell growth arrest and antimicrobial activity. We investigated CP activity and its possible apoptosis-inducing mechanism of action against an antiandrogen therapy-resistance prostate cancer cell line LNCaP. Cell viability and Annexin V FITC assays were performed in order to investigate its cell death activity and apoptosis, respectively. In order to address cell death inducing mechanism(s), immunocytochemistry and immunobloting analysis, reactive oxygen species (ROS) and nitric oxide (NO) measurements were performed. The effective concentration of CP against LNCaP promoting LNCaP cell death was 200 µg/mL. ROS and NO levels of cells remarkably were enhanced following treatment with 50 and 100 µg/mL of CP, respectively. Protein expression of anti-apoptotic protein survivin was significantly decreased after administration of tumor cells with CP. Our data indicate that CP regulates the LNCaP cells viability via survivin-mediated pathway and ROS and NO enhancement. Thus, inhibition of survivin expression, enhancement of ROS and NO level by CP or other similar pharmaceutical agents might be effective in lowering the malignant proliferation of human prostate cancer cells.
['Sattari|Mina|M|', 'Pazhang|Yaghub|Y|', 'Imani|Mehdi|M|']
D017209:Apoptosis D045744:Cell Line, Tumor D006801:Humans D051034:Inhibitor of Apoptosis Proteins D039841:Leukocyte L1 Antigen Complex D008297:Male D009504:Neutrophils D009569:Nitric Oxide D011471:Prostatic Neoplasms D017382:Reactive Oxygen Species D000077022:Survivin
calprotectin LNCaP survivin apoptosis reactive oxygen species nitric oxide