NTPDase5/PCPH as a New Target in Highly Aggressive Tumors: A Systematic Review
Figure 2
Integration of the proposed pathways by which the NTPDase5/mt-PCPH acts on the neoplastic progression. Due to the lack of information about the role of these proteins in cancer development and progression, this scheme presents all data published so far, not taking into consideration in which cell the proposed mechanisms were studied although it is possible that some of the contradictions presented may be a direct consequence of this fact. The figure demonstrates how the loss of the tumor suppressor PTEN possibly causes an increase in NTPDase5 expression and an overactive PI3K/AKT pathway. AKT and mTOR regulate cell growth and survival, such as Bcl-2 gene leading to an increase in apoptotic resistance. Furthermore it is also suggested that the NTPDase5 interacts with PKCδ, upregulating its levels and inducing cancer cell invasiveness. pP53, pPKCα, and pBcl-2 are the phosphorylated forms of the respective proteins and correspond to the phosphorylation of p53 at Ser18, pPKC at Trh638, and Bcl-2 at Ser70.
