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Int J Mol Med. 2014 Aug;34(2):399-408. doi: 10.3892/ijmm.2014.1812. Epub 2014 Jun 17.

Suppression of PAX6 promotes cell proliferation and inhibits apoptosis in human retinoblastoma cells.

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Beijing Institute of Ophthalmology, Beijing Tongren Hospital, Capital Medical University, Beijing 100005, P.R. China.
Department of Microbiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, P.R. China.


The aim of this study was to investigate the role of the transcription factor, PAX6, in the development of retinoblastoma. The expression of endogenous PAX6 was knocked down using PAX6-specific lentivirus in two human retinoblastoma cell lines, SO-Rb50 and Y79. Cell proliferation functional assays and apoptotic assays were performed on the cells in which PAX6 was knocked down. The results revealed that PAX6 knockdown efficiency was significant (P<0.01, n=3) in the SO-Rb50 and Y79 cells. The inhibition of PAX6 reduced tumor cell apoptosis (P<0.05, n=3), but induced cell cycle S phase arrest (SO-Rb50; P<0.05, n=3) and G2/M phase arrest (Y79; P<0.05, n=3). Western blot analysis indicated that the inhibition of PAX6 increased the levels of the anti-apoptotic proteins, Bcl-2, proliferating cell nuclear antigen (PCNA) and CDK1, but reduced the levels of the pro-apoptotic proteins, BAX and p21. In conclusion, our data demonstrate that the suppression of PAX6 increases proliferation and decreases apoptosis in human retinoblastoma cells by regulating several cell cycle and apoptosis biomarkers.

[Indexed for MEDLINE]
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