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Gene silencing of translationally controlled tumor protein (TCTP) by siRNA inhibits cell growth and induces apoptosis of human prostate cancer cells.
- Source :
-
International journal of oncology [Int J Oncol] 2009 May; Vol. 34 (5), pp. 1241-6. - Publication Year :
- 2009
-
Abstract
- Translationally controlled tumor protein (TCTP) is a novel anti apoptotic protein which is highly expressed in several cancer cell types including prostate cancer. However, studies investigating the role of TCTP in prostate cancer are scarce. Therefore, in this study we evaluated the effect of small interference RNA (siRNA) based knocking down of TCTP gene in prostate cancer cells. Cell proliferation and apoptosis were evaluated. Our results showed that TCTP is highly expressed in LNCaP cells compared to normal prostate epithelial cells. Transfection with TCTP siRNA specifically and drastically reduced the expression of both mRNA and protein levels of TCTP in LNCaP cells. The decreased expression of TCTP was associated with decreased viability of LNCaP cells. Further analysis of the transfected LNCaP cells showed that they undergo apoptosis via caspase-8 and caspase-3 dependent pathways. Results presented herein suggest a potential therapeutic application for prostate cancer by targeting TCTP gene using an siRNA approach.
- Subjects :
- Biomarkers, Tumor genetics
Caspase 3 metabolism
Caspase 8 metabolism
Cell Survival drug effects
Cell Survival genetics
Cells, Cultured
Down-Regulation drug effects
Drug Evaluation, Preclinical
Gene Expression Regulation, Neoplastic drug effects
Gene Silencing physiology
Humans
Male
Prostatic Neoplasms genetics
Tumor Protein, Translationally-Controlled 1
Apoptosis drug effects
Biomarkers, Tumor antagonists & inhibitors
Cell Proliferation drug effects
Prostatic Neoplasms pathology
RNA, Small Interfering pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 1019-6439
- Volume :
- 34
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- International journal of oncology
- Publication Type :
- Academic Journal
- Accession number :
- 19360337