PTEN

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Annexin A2 Regulates AKT Upon H₂O₂-Dependent Signaling Activation in Cancer Cells

 

Authors and Affiliations:

Castaldo SA1, , Ajime T1, Serrão G1, Anastácio F1, Rosa JT1, Giacomantonio CA2, Howarth A3, Hill R1,3, and Madureira PA1, 3

1 Centre for Biomedical Research (CBMR), Campus of Gambelas, University of Algarve, Building 8, Room 2.22, 8005-139 Faro, Portugal;

2 Department of Medicine, Dalhousie University, Halifax, Nova Scotia B3H 4R2, Canada;

A proteína anexina A2 regula a proteína AKT em resposta à ativação de vias de sinalização dependentes de H2O2 em células cancerígenas

Com este trabalho o nosso grupo de investigação descobriu que a proteína anexina A2 (ANXA2) tem um papel importante na regulação de uma das principais vias de sinalização celular envolvida na promoção tumoral/oncogénese, nomeadamente a via PI3K/AKT. Isto acontece através da interação entre a ANXA2 e a proteína PTEN, que constitui o principal inibidor da via PI3K/AKT; o que leva à ativação de PTEN e subsequentemente inativação da proteína AKT.

Prostate cancer prognosis defined by the combined analysis of 8q, PTEN and ERG

Prostate cancer (PCa) is the second most frequently diagnosed non-skin cancer in men worldwide and the fifth cause of cancer-related deaths. The introduction of serum prostate-specific antigen (PSA) analysis constituted an important clinical tool for early PCa detection and disease monitoring, but this test has modest sensitivity and specificity and has limited prognostic value. This shows that there is an unmet need of novel diagnostic and prognostic markers for PCa clinical management.

«Making cells ignore mutations could treat genetic diseases» in New Scientist

Citing Michael Le Page in «New Scientist»:

«In many diseases, including cancer, DNA mutations create a stop codon in the wrong place. A single mutation can truncate a protein that should be 100 amino acids long to one that is just 15 long, rendering it completely useless. These are known as nonsense mutations, and they cause about 10 per cent of all genetic diseases.

It’s possible to make artificial tRNAs that recognise a premature stop codon, and instead of terminating the protein-making process, add the amino acid required to make a useful protein.

«Making cells ignore mutations could treat genetic diseases» in New Scientist

Citing Michael Le Page in «New Scientist»:

«In many diseases, including cancer, DNA mutations create a stop codon in the wrong place. A single mutation can truncate a protein that should be 100 amino acids long to one that is just 15 long, rendering it completely useless. These are known as nonsense mutations, and they cause about 10 per cent of all genetic diseases.

It’s possible to make artificial tRNAs that recognise a premature stop codon, and instead of terminating the protein-making process, add the amino acid required to make a useful protein.