Salvianolic acid A positively regulates PTEN protein level and inhibits growth of A549 lung cancer cells

被引:34
作者
Bi, Lei [1 ]
Chen, Jianping [2 ]
Yuan, Xiaojing [2 ]
Jiang, Zequn [2 ]
Chen, Weiping [2 ]
机构
[1] Nanjing Univ Chinese Med, Associated Hosp, Nanjing 210046, Jiangsu, Peoples R China
[2] Nanjing Univ Chinese Med, Coll Basic Med, 138 Xianlin Rd, Nanjing 210046, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
salvianolic acid A; apoptosis; phosphatase and tensin homolog; Akt phosphorylation;
D O I
10.3892/br.2012.33
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 [基础医学];
摘要
Salvianolic acid A (Sal A) is an effective compound extracted from Salvia miltiorrhiza which has been used in the treatment of various diseases. Preliminary data indicate that Sal A treatment has a specific anti-lung cancer effect. However, the manner in which Sal A regulates cancer growth remains unknown. In this study, the A549 lung cancer cell line and its response to Sal A treatment was examined. Results showed that Sal A treatment significantly decreased A549 cell growth, promoted partial apoptosis and increased mitochondrial membrane permeability. Western blot analysis showed that Sal A upregulated the phosphatase and tensin homolog (PTEN) protein level, while consistently downregulating Akt phosphorylation. These results indicate that Sal A negatively mediates A549 lung cancer cell line growth or apoptosis, most likely by positively regulating PTEN protein level.
引用
收藏
页码:213 / 217
页数:5
相关论文
共 16 条
[1]
The PTEN/PI3K/AKT signalling pathway in cancer, therapeutic implications [J].
Carnero, Amancio ;
Blanco-Aparicio, Carmen ;
Renner, Oliver ;
Link, Wolfgang ;
Leal, Juan F. M. .
CURRENT CANCER DRUG TARGETS, 2008, 8 (03) :187-198
[2]
Chu EC, 2004, MED SCI MONITOR, V10, pRA235
[3]
Akt inhibition promotes autophagy and sensitizes PTEN-null tumors to lysosomotropic agents [J].
Degtyarev, Michael ;
De Maziere, Ann ;
Orr, Christine ;
Lin, Jie ;
Lee, Brian B. ;
Tien, Janet Y. ;
Prior, Wei W. ;
van Dijk, Suzanne ;
Wu, Hong ;
Gray, Daniel C. ;
Davis, David P. ;
Stern, Howard M. ;
Murray, Lesley J. ;
Hoeflich, Klaus P. ;
Klumperman, Judith ;
Friedman, Lori S. ;
Lin, Kui .
JOURNAL OF CELL BIOLOGY, 2008, 183 (01) :101-116
[4]
Requirement of Phosphatidylinositol(3,4,5)Trisphosphate in Phosphatidylinositol 3-Kinase-Induced Oncogenic Transformation [J].
Denley, Adam ;
Gymnopoulos, Marco ;
Kang, Sohye ;
Mitchell, Christina ;
Vogt, Peter K. .
MOLECULAR CANCER RESEARCH, 2009, 7 (07) :1132-1138
[5]
Induction of Akt Activity by Chemotherapy Confers Acquired Resistance [J].
Huang, Wei-Chien ;
Hung, Mien-Chie .
JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION, 2009, 108 (03) :180-194
[6]
PTEN expression in breast and endometrial cancer:: Correlations with steroid hormone receptor status [J].
Kappes, H ;
Goemann, C ;
Bamberger, AM ;
Löning, T ;
Milde-Langosch, K .
PATHOBIOLOGY, 2001, 69 (03) :136-142
[7]
AKT1, AKT2 and AKT3-dependent cell survival is cell line-specific and knockdown of all three isoforms selectively induces apoptosis in 20 human tumor cell lines [J].
Koseoglu, Sandra ;
Lu, Zhuomei ;
Kumar, Chandra ;
Kirschmeier, Paul ;
Zou, Jun .
CANCER BIOLOGY & THERAPY, 2007, 6 (05) :755-762
[8]
Crystal structure of the PTEN tumor suppressor: Implications for its phosphoinositide phosphatase activity and membrane association [J].
Lee, JO ;
Yang, HJ ;
Georgescu, MM ;
Di Cristofano, A ;
Maehama, T ;
Shi, YG ;
Dixon, JE ;
Pandolfi, P ;
Pavletich, NP .
CELL, 1999, 99 (03) :323-334
[9]
PTEN function: how normal cells control it and tumour cells lose it [J].
Leslie, NR ;
Downes, CP .
BIOCHEMICAL JOURNAL, 2004, 382 :1-11
[10]
Role of PTEN and Akt in the regulation of growth and apoptosis in human osteoblastic cells [J].
Nielsen-Preiss, SM ;
Silva, SR ;
Gillette, JM .
JOURNAL OF CELLULAR BIOCHEMISTRY, 2003, 90 (05) :964-975