Presentation Type: Poster
Abstract: Introduction: Centrosomal protein of 55 kDa (CEP55) is a centrosome and mid-body associated mitotic phosphoprotein that plays a key role in cytokinesis, the final stage of cell division. Our laboratory identified that CEP55 is involved in maintenance of genome stability and integrity, which if dysregulated, can lead to cancer. Over-expression of this protein promotes tumor survival and progression and has been reported in many cancers including breast cancer. While siRNA based knockdown studies have provided clues about the critical role of Cep55 in the regulation of Cytokinesis,
Material and Methods: Cep55 knockout (KO) model has been generated to examine physiological role of Cep55. This KO mouse model used to validate whether Cep55 loss can prevent tumor development and/or progression to characterize the role of Cep55 in cancer. The first knockout allele approach was used to create Cep55 KO mice. This strategy relies on the identification of a critical exon common to all transcript variants that, when deleted, creates a frame-shift mutation.
Results: Several intercrosses of Cep55 heterozygous mice demonstrated that all pups were wildtype or heterozygous in genotyping and no homozygous pups have been obtained, indicating that homozygous Cep55 deletion may lead to embryonic lethality. Generating the Mouse Embryonic Fibroblast lines for in vitro investigations can clarify the molecular mechanism of this clue.
Conclusion: CEP55 is an essential gene for embryonic viability where both alleles depletion resulted in lethality and this makes the oncogene reliable target for treating breast cancer.