THE ROLE OF miR-204 AND NOD1 RECEPTOR IN PROSTATE CANCER INFLAMMATION SIGNALLING

Micro RNA miR-204 has a role in prostate cancerogenesis and metastasis. For the first time it is implicated in the modulation of innate inflammatory signalling in prostate cancer. The effect of miR-204 mimic transfection on Gram-synthetic bacterial peptidoglycan challenged human prostate cancer cell lines LNCaP (p53(+/+), AR(+)) and PC3 (p53(-/-), AR(-)) was evaluated using flow cytometric (FCS) and immunocytochemical detection of the expression of NOD1. Peptidoglycan challenge effects were modulated by miR-204 mimic towards upregulation of NOD1 (LNCaP, PC3) affecting the innate to autophagy signalling (FCS). miR-204 artificial over-expression (mimic) significantly stratified the two cancer phenotype models. Inflammatory signalling was overall depressed in PC3, effect reversed by miR-204, while in LNCaP it had no effect on peptidoglycan challenge. The FCS observed differences were validated using immunocytochemistry. Our data suggest that miR-204 significantly impacts already altered innate immunity signalling in prostate cancer cells, potentiating inflammatory challenge induced innate receptors - NOD1.