Investigation of the involvement of PRL in the PI3K/Akt signaling pathway during Drosophila eye development

• Main Authors: Zih-Yuan Shen, 沈子元
• Other Authors: Ming-Der Lin
• Format: Others
• Language: zh-TW
• Published: 2011
• Online Access: http://ndltd.ncl.edu.tw/handle/51874359948904963758

碩士 === 慈濟大學 === 生命科學系碩士班 === 99 === Phosphatase of regenerating liver (PRL) protein family showed high degree of correlation with cancer metastasis and it has been considered as a potential target for cancer therapy. However, PRL substrate has not yet been identified and its function in development is still unclear. PRL is highly conserved in among species. In Drosophila genome, it has only one PRL gene with about 70％ similarity to its human homologs, hPRL1, 2, and 3. Previous studies in our lab indicated that dmPRL knockdown caused cell death during Drosophila eye development. In this study we demonstrate that the phenotype of dmPRL knockdown can be rescued by overexpression of hPRL3 or zfPRL2. It has been shown that the PTEN and PI3K/Akt signaling pathways regulate cell proliferation and cell growth during Drosophila eye development. In human cancer cell lines, it has been found that hPRL can paticipate in the regulation of the PTEN/PI3K-Akt signaling. To test the genetic interaction of dmPRL and the PTEN/PI3K-Akt pathway during Drosophila eyes development, we constructed several versions of dmPRL mutant proteins. Our results indicate that dmPRL could be involved in the regulation of the PTEN/PI3K-Akt pathway. In proliferating cell, dmPRL overexpression can suppress the small eyes phenotype caused by overexpression of dPTEN or Dp110D954A. In differentiating cells, dmPRL not only affects the growth signal of the PI3K/Akt pathway, but also regulates cell death through signaling pathways which independent of the PI3K/Akt signaling.