Activation of nuclear PTEN by inhibition of Notch signaling induces G2/M cell cycle arrest in gastric cancer

• Published in: Oncogene Vol. 35; no. 2; pp. 251 - 260
• Main Authors: Kim, S-J, Lee, H-W, Baek, J-H, Cho, Y-H, Kang, H G, Jeong, J S, Song, J, Park, H-S, Chun, K-H
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 14.01.2016; Nature Publishing Group
• Subjects: 13/1; 13/105; 13/109; 13/2; 13/31; 13/89; 13/95; 14; 631/67/1504/1829; 64/60; Animals; Apoptosis; Apoptosis - drug effects; Apoptosis - genetics; Cancer therapies; Cell Biology; Cell cycle; Cell Line, Tumor; Cell Nucleus - metabolism; Cellular signal transduction; Chemotherapy; Cyclin B1; Cyclin B1 - metabolism; Dephosphorylation; Development and progression; Female; G2 Phase Cell Cycle Checkpoints - drug effects; Gastric cancer; Gene Expression Regulation, Neoplastic; Gene mutations; Genetic aspects; Health aspects; Human Genetics; Humans; Internal Medicine; Kinases; Localization; Medicine; Medicine & Public Health; Mice, Inbred BALB C; Mutation; Notch1 protein; Oligopeptides - pharmacology; Oncology; original-article; Phosphorylation; PTEN Phosphohydrolase - genetics; PTEN Phosphohydrolase - metabolism; PTEN protein; Receptor, Notch1 - genetics; Receptor, Notch1 - metabolism; Receptors, Notch - genetics; Receptors, Notch - metabolism; Secretase; Signal Transduction; siRNA; Stomach cancer; Stomach Neoplasms - drug therapy; Stomach Neoplasms - metabolism; Stomach Neoplasms - mortality; Stomach Neoplasms - pathology; Toxicity; Tumor suppressor genes; Tumorigenesis; Tumors; Xenograft Model Antitumor Assays; Xenografts

Mutation in PTEN has not yet been detected, but its function as a tumor suppressor is inactivated in many cancers. In this study we determined that, activated Notch signaling disables PTEN by phosphorylation and thereby contributes to gastric tumorigenesis. Notch inhibition by small interfering RNA...