Ribosomal protein P2: a potential molecular target for antisense therapy of human malignancies.
BACKGROUND: Ribosomal protein P2 is an important component of protein translation machinery. We hypothesized that antisense-mediated depletion may disrupt the proteome of cancer cells. This study includes experiments to ascertain whether this could be a useful approach for cancer therapies. MATERIALS AND METHODS: MIA PaCa-2 and BxPC-3 cells were transfected with P2-antisense oligonucleotide or controls. Growth was assayed using MTT. Protein P2 was measured using Western blotting. Proteomes were compared using two-dimensional electrophoresis and changes were characterized by mass spectrometry. A macroarray was used to identify cancers which may be vulnerable. RESULTS: Antisense-P2 reduced P2 levels by 63% (p < 0.05) and inhibited BxPC-3 growth to 65% of control (p < 0.05). Seventeen (5.4%) proteins changed on two-dimensional electrophoresis including Rho C, translationally-controlled tumor protein, vinculin, LDH, ribosomal protein L23a, F-actin capping protein and eIF-3. Breast cancer underexpressed P2 compared to normal tissue (p < 0.001). CONCLUSION: Antisense-P2 technology has potential to slow growth of cancer cells. This effect is mediated through multiple proteomic changes.[1]References
- Ribosomal protein P2: a potential molecular target for antisense therapy of human malignancies. Gardner-Thorpe, J., Ito, H., Ashley, S.W., Whang, E.E. Anticancer Res. (2003) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
