siRNA knockdown of ribosomal protein gene RPL19 abrogates the aggressive phenotype of human prostate cancer

Ribosomal protein RPL19 is an integral component of eukaryotic ribosomes and universally involved in protein synthesis. Although consistently stable  in normal cells, RPL19 transcription is relatively elevated in prostate cancer. Using siRNA, we inhibited RPL19 transcription and demonstrated the gene to be functionally involved in promoting the malignant phenotype. Reducing RPL19 modulates a subset of genes rather than globally down-regulating protein synthesis, as evidenced by Western blotting and maintenance of cell proliferation. Mechanistically, either all ribosomes are not structurally and functionally identical or absence of RPL19 is compensated by other ribosomal protein genes. Following RPL19 inhibition, gene expression analysis confirms induction of the non-malignant phenotype principally to involve perturbation of transcription factor networks and cellular adhesion genes. 10 microarray experiments were analysed using five different prostate cell types: PC3M, PNT2, PC3M with stable knockdown transfection, PC3M with a scrambled virus and various PC3M knockdowns pooled