TY - JOUR AB - Colorectal cancer is one of the most common malignancies in the world. Overactivity of phosphatidylinositol 3-kinase (PI3K) is frequently detected in colorectal carcinoma. PI3K signaling plays a pivotal role in intracellular signal transduction pathways involved in cell growth, cellular transformation, and tumorigenesis. To specifically inhibit PI3K activity in colorectal cancer cells, we constructed a siRNA against the PI3K regulatory subunit p85α and transfected it into LoVo and SW480 cells. In the present study, treatment of colorectal cancer cells with PI3K p85α-specific siRNA inhibited cell proliferation, induced G1 phase cell cycle arrest and sensitized colorectal cancer cells to 5-FU-induced apoptosis. Furthermore, depletion of PI3K p85α resulted in significant activation of three Forkhead box class O (FoxO) transcription factors, which inhibited the expression of cyclin D1, cdk4 and induced expression of p27/Kip1. Activation of FoxO transcription factors also increased the expression of FasL. Thus, our results indicate that siRNA-mediated gene silencing of PI3K p85α may be a useful therapeutic strategy for colorectal carcinoma. AD - Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P.R. China null AU - Sun,Yan AU - Zhao,Shiyi AU - Tian,Hua AU - Xie,Xiaoyun AU - Xiao,Faman AU - Li,Kang AU - Song,Yugang DA - 2009/12/01 DO - 10.3892/or_00000585 EP - 1441 IS - 6 JO - Oncol Rep PY - 2009 SN - 1021-335X 1791-2431 SP - 1435 ST - Depletion of PI3K p85α induces cell cycle arrest and apoptosis in colorectal cancer cells T2 - Oncology Reports TI - Depletion of PI3K p85α induces cell cycle arrest and apoptosis in colorectal cancer cells UR - https://doi.org/10.3892/or_00000585 VL - 22 ER -