Dear Editor,Class I PI3Ks play a central role in cancer progression via its downstream signaling nodes(GSK3,FOXO,mTORC1,etc.).1 Under physiological conditions,the catalytic p110 subunit is stabilized and inhibited by ...Dear Editor,Class I PI3Ks play a central role in cancer progression via its downstream signaling nodes(GSK3,FOXO,mTORC1,etc.).1 Under physiological conditions,the catalytic p110 subunit is stabilized and inhibited by the regulatory p85 subunit in the cytoplasm.1,2 In cancer cells,PI3K activity is aberrantly regulated mostly through excessive upstream growth signals,disinhibition of p110 by genetic alteration of PI3K genes,and deficiency of the phosphatase PTEN.1 Protein interactions between PI3K and overexpressed oncoproteins such as Ras also account for the activation of PI3K in cancer cells.1 Abnormally activated PI3K/AKT pathway is a popular drug target for cancer therapy;therefore,the mechanisms underlying the regulation of PI3K activity need the elaborate exploration.展开更多
基金supported by the National Natural Science Foundation of China(81872354,81790254 and 81572827)to W.H.
文摘Dear Editor,Class I PI3Ks play a central role in cancer progression via its downstream signaling nodes(GSK3,FOXO,mTORC1,etc.).1 Under physiological conditions,the catalytic p110 subunit is stabilized and inhibited by the regulatory p85 subunit in the cytoplasm.1,2 In cancer cells,PI3K activity is aberrantly regulated mostly through excessive upstream growth signals,disinhibition of p110 by genetic alteration of PI3K genes,and deficiency of the phosphatase PTEN.1 Protein interactions between PI3K and overexpressed oncoproteins such as Ras also account for the activation of PI3K in cancer cells.1 Abnormally activated PI3K/AKT pathway is a popular drug target for cancer therapy;therefore,the mechanisms underlying the regulation of PI3K activity need the elaborate exploration.
