Abstract
To evaluate the effect of exogenous wild PTEN gene stable transfected into human ovarian cancer cell line HO-8910 on phosphatidyl inositol 3-kinase (PI3K)/protein kinase B (Akt) signal pathway and cells proliferation. Wild-type PTEN recombinant eukaryotic expression plasmid was constructed and then was transfected into HO-8910 cells by lipofectamine 2000. The expression of PTEN, Akt1, Akt2, PI3K mRNA and protein of PTEN were tested by reverse transcription (RT)-PCR and Western blot. The proliferation of HO-8910 after wild PTEN gene transfected was measured by methyl thiazolyl tetrazolium (MTT). Wild-type PTEN gene was successfully transfected into HO-8910 cells. The results of RT-PCR and western bolt showed that there were the significant expression high level of PTEN mRNA and protein after infected by wild-PTEN plasmid than those in the control [(17,372 ± 23) vs. (39 ± 1) vs. (78 ± 4) copies/ml, P < 0.05]. While the expression of mRNA of Akt1, Akt2 and PI3K were decreased clearly than those in the control [(28 ± 2) vs. (115 ± 5), (7 ± 1) vs. (18 ± 2), (61 ± 2) vs. (84 ± 2) copies/ml, all P < 0.05]. The proliferation rate of HO-8910 cells was obviously slower than those in the control (90 158 ± 47 vs. 148,251 ± 65 vs. 250,115 ± 62, P < 0.05). Transfection of PTEN may increase the expression of PTEN and inhibit the proliferation of HO-8910 cells, in which PI3K/Akt signal pathway is inhibit significantly.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
