Regulatory mechanisms of PI3K/AKT signaling pathway in acute leukemia.
- Author:
Wei-Li WANG
1
;
Ying-Chi ZHANG
;
Hui-Min ZENG
;
Chun-Lan HUA
;
Wei WEI
;
Jin XU
;
Xiao-Fan ZHU
;
Tao CHENG
;
Wei-Ping YUAN
Author Information
1. Chinese Academy of Medical Sciences, Tianjin, China.
- Publication Type:Journal Article
- MeSH:
Carrier Proteins;
genetics;
metabolism;
Case-Control Studies;
Cyclin D1;
genetics;
metabolism;
Forkhead Box Protein O1;
Forkhead Transcription Factors;
genetics;
metabolism;
Gene Expression Regulation, Leukemic;
Humans;
Leukemia;
genetics;
metabolism;
PTEN Phosphohydrolase;
genetics;
metabolism;
Proto-Oncogene Proteins c-akt;
metabolism;
RNA, Messenger;
genetics;
Rapamycin-Insensitive Companion of mTOR Protein;
Signal Transduction;
TOR Serine-Threonine Kinases;
genetics;
metabolism;
Transcriptome
- From:
Journal of Experimental Hematology
2012;20(1):18-21
- CountryChina
- Language:Chinese
-
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.
