| First Author | Jiang T | Year | 2016 |
| Journal | Mol Med Rep | Volume | 13 |
| Issue | 3 | Pages | 2039-45 |
| PubMed ID | 26782701 | Mgi Jnum | J:320217 |
| Mgi Id | MGI:6869021 | Doi | 10.3892/mmr.2016.4762 |
| Citation | Jiang T, et al. (2016) Knockout of phospholipase Cepsilon attenuates N-butyl-N-(4-hydroxybutyl) nitrosamine-induced bladder tumorigenesis. Mol Med Rep 13(3):2039-45 |
| abstractText | Bladder cancer frequently shows mutational activation of the oncogene Ras, which is associated with bladder carcinogenesis. However, the signaling pathway downstream of Ras remains to be fully elucidated. N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) is able to induce bladder cancer by driving the clonal expansion of initiated cells carrying the activated form of Ras. Phospholipase Cepsilon (PLCepsilon) is the main target of BBN, while the tumor promoting role of PLCepsilon remains controversial. The present study examined the role of PLCepsilon in BBNinduced bladder carcinogenesis of mice with genetically inactivated PLCepsilon. Using light and electron microscopy, the present study demonstrated that PLCepsilon(/) mice were resistant to BBNinduced bladder carcinogenesis. Furthermore, it was demonstrated that cyclooxygenase 2 and vascular endothelial growth factorA were affected by the PLCepsilon background of the mice, suggesting that the role of PLCepsilon in tumor promotion may be ascribed to augmentation of inflammatory responses and angiogenesis. These results indicated that PLCepsilon is crucial for BBNinduced bladder carcinogenesis as well as signaling downstream of Ras, and that PLCepsilon is a candidate molecular target for the development of anti-cancer drugs. |
