title: [Regulatory mechanisms of PI3K/AKT signaling pathway in acute leukemia].
abstract: This study was aimed to analyze the expression profiles of PI3K/AKT signaling pathway genes from bone marrow samples of AML and ALL patients and normal samples. AML, ALL and normal bone marrow samples were collected from 6 AML, 6 ALL patients and 4 normal persons. The expression of PI3K/AKT signaling pathway genes including PTEN, CCND1, mTOR, RICTOR, FOXO1 were detected by real-time fluorescent quantification RT-PCR while GAPDH gene expression was used as an internal reference. The relative gene expression level was calculated by the method of the 2(-ΔΔCt). The results showed that the gene expression profiles were different between normal and leukemic groups. PTEN, mTOR and RICTOR expression levels were down-regulated, while FOXO1 and CCND1 levels were up-regulated in AML and ALL. PTEN was down-regulated in 10 out of the 12 samples; mTOR was down-regulated in 9 out of the 12 samples; RICTOR was down-regulated in 7 out of the 12 samples; FOXO1 was up-regulated in 9 out of the 12 samples and CCND1 was up-regulated in 7 out of the 12 samples. It is concluded that PI3K/AKT signal pathway is activated in both AML and ALL leukemic cells.
authors.affiliation: Chinese Academy of Medical Sciences, Tianjin, China.
authors.forename: Wei-Li
authors.initials: WL
authors.lastname: Wang
authors.forename: Ying-Chi
authors.initials: YC
authors.lastname: Zhang
authors.forename: Hui-Min
authors.initials: HM
authors.lastname: Zeng
authors.forename: Chun-Lan
authors.initials: CL
authors.lastname: Hua
authors.forename: Wei
authors.initials: W
authors.lastname: Wei
authors.forename: Jin
authors.initials: J
authors.lastname: Xu
authors.forename: Xiao-Fan
authors.initials: XF
authors.lastname: Zhu
authors.forename: Tao
authors.initials: T
authors.lastname: Cheng
authors.forename: Wei-Ping
authors.initials: WP
authors.lastname: Yuan
mesh_terms: D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D016022:Case-Control Studies; D019938:Cyclin D1 / Q000235:genetics / Q000378:metabolism; D000071161:Forkhead Box Protein O1; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D015973:Gene Expression Regulation, Leukemic; D006801:Humans; D007938:Leukemia / Q000235:genetics / Q000378:metabolism*; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D000076226:Rapamycin-Insensitive Companion of mTOR Protein; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D059467:Transcriptome
chemical_list: C530104:CCND1 protein, human; D002352:Carrier Proteins; C085126:FOXO1 protein, human; D000071161:Forkhead Box Protein O1; D051858:Forkhead Transcription Factors; C492571:RICTOR protein, human; D012333:RNA, Messenger; D000076226:Rapamycin-Insensitive Companion of mTOR Protein; D019938:Cyclin D1; C546842:MTOR protein, human; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human