Rashvand Zahra, Heidari Mansour, Raoofian Reza, Modarresi Mohammad Hossein, Shirkoohi Reza
1. Dept. of Medical Genetics, Tehran University of Medical Sciences (TUMS) , Tehran, Iran.
1. Dept. of Medical Genetics, Tehran University of Medical Sciences (TUMS) , Tehran, Iran ; 2. Stem Cell Preparation Unit, Farabi Eye Hospital, Tehran University of Medical Sciences , Tehran, Iran.
Iran J Public Health. 2013 Nov;42(11):1242-52.
BACKGROUND: TGIFLX, a Homoproteins cluster member located on the X chromosome, has a critical role in male reproduction and prostate development. Previous studies have shown the erratic expression of TGIFLX gene in a large proportion of prostate tumors. However TGIFLX function in prostate development remains unknown. The purpose of this study was to evaluate the consequences of TGIFLX expression on prostate cancer cell lines (LNCaP). METHOD: Inducible Tet-On gene expression system was used with a regulatory capability by doxycycline induction. In this system, stable LNCaP cells with TGIFLX tet-on plasmid were able to induce TGIFLX expression by doxycycline treatment. TGIFLX gene expression was confirmed by RT-PCR. RESULTS: Induction of gene expression caused cell proliferation decrement and apoptosis increment in LNCaP TGIFLX cells compared with control cells (P<0.01). Also, by using PEGFPN1 plasmid protein in this study localization was shown in nucleus. The gene was cloned in the plasmid and transfected to LNcap cells with plasmid PEGFPN1 TGIFLX and the plasmid was PEGFPN1. The TGIFLX expression was confirmed by RT-PCR and fluorescent microscopy. CONCLUSION: TGIFLX expression demonstrated a tumor suppressor characterization in a prostatic cancer cell line with low grade of tumorigenicity (LNCaP). More cell lines with different level of tumorogenicity need to be investigated for further clarification of the TGIFLX gene function.
Iran J Public Health. 2013-11
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