The role of E17k AKT mutation in breast cancers
Background:
Tumorigenesis involves the alternation of cell signaling, resulting in unrestrained cell proliferations and cell survivals. The interruption of PI3K/AKT signaling pathway has previously shown to play a significant role leading to cancer development. This pathway is stimulated when growth factor encodes the receptor tyrosine kinase, which phosphorylates the phosphoinositide 3-kinase (PI3K) consisting of p85 and p110 subunits (Figure 1). The phosphorylation of PI3K would further phosphorylate phosphatidylinositol 4,5 diphosphates (Ptdins(4,5)P2) at the Carbon 3 position of the lipid to allow the production of phosphatidylinositol 3,4,5 triphosphates (Ptdin(3,4,5)P3). This lipid is plasma membrane bound and targets proteins with pleckstrin-homology (PH) domains, such as AKT, PDK1, mTORC2 complex and Rho GEFs. However, the activation of AKT singnalling pathway requires the upstream activators, PDK1 and mTORC2 complex to phosphorylate threonine 308 and serine 473 of AKT, respectively.
Figure 1. Regulation of the PI3K/AKT signalling pathway.
Upon the activation of AKT, the translocation of AKT from the nucleus and cytoplasm takes place to the plasma membrane. This movement promotes further downstream phosphorylation of the effector proteins, leading to the activation or inhibition of the specific effector proteins, which will have an effect on cystoskeletal rearrangements, migration, proliferation or survival of the cell.
During PI3K/AKT signalling, the pathways can be interrupted by many inhibition factors. These include gene overexpression, deletion, amplification and mutation, which could all induce pathological diseases that increases cell proliferation, inhibits ...
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...lts of both papers, it suggests that AKT as a major mediator in altering the signaling pathway of PI3K/AKT leading to ocogenesis. The mutation E17K in AKT1 does pose a role in cancer development by the promotion of AKT phosphorylation. However, in order to achieve this phenotype, the co-occurrence of additional mutation or genetic events despite from E17K, may also be present.
Future directions:
The findings of Carpten et al. and Lauring et al. have both made implications to therapeutic purposes in relation to ocogenesis of breast cancers. In future studies, the identification of other cooperative genetic factors in causing tumorgenesis could be examined in order to gain advance knowledge of cancer development. As the result, their corporations with AKT mutation can be observed to suggest further implications on the treatment and prevention of human cancers.
ARTICLE AUTHOR, TITLE AND SOURCE: Fiske, Jo-Anne. "Gender and the Paradox of Residential Education in Carrier Society." in Christine Miller and Patricia Chuchryk, Women of the First Nations: Power, Wisdom, Strength. Winnipeg: U of Manitoba, 1996. 167-82. Topic: Jo-Anne Fiske’s article explores the paradoxical consequences of residential education on the women of the Carrier society in central British Columbia. Her chapter focuses on contradictory outcomes of formal colonial schooling by analyzing
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