Inhibition of proliferation of rat lens epithelial cell by overexpession of KLF6

被引：0

作者：

Su, Ying ^{[1
,2
]}

Wang, Feng ^{[1
,2
,3
]}

Zhou, Dan ^{[1
]}

Gao, Weiqi ^{[1
]}

Hu, Qi ^{[1
]}

Cui, Hao ^{[1
]}

Zhang, Jie ^{[2
,3
]}

机构：

[1] Harbin Med Coll, Clin Coll 1, Dept Ophthalmol, Harbin 150001, Peoples R China

[2] Univ Nebraska Med Ctr, Dept Ophthalmol, Omaha, NE USA

[3] Univ Nebraska, Redox Biol Ctr, Lincoln, NE USA

来源：

MOLECULAR VISION | 2011年 / 17卷 / 122期

关键词：

POSTERIOR CAPSULE OPACIFICATION; ZINC-FINGER PROTEIN; OVARIAN-CANCER; GROWTH; PROGRESSION; PROMOTER; GENES; BRCA1; RISK; BETA;

D O I：

暂无

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Purpose: Proliferation of lens epithelial cell (LEC) is main principle for posterior capsular opacity (PCO) following surgery. We investigated whether overexpression of Kruppel-like factor 6 (KLF6) can be employed to increase protein 21 (p21) and protein 27 kinase inhibition protein 1 (p27(kip1)) levels and its effect on proliferation of LEC. Methods: A plasmid containing KLF6 cDNA was used to increase the level of KLF6 protein in rat lens epithelial cells (rLEC) which can lead to consequent degradation of p21 and p27(kip1). Cell proliferation was assayed by cell counts and bromodeoxyuridine (BrdU) Incorporation. Results: western blot analysis showed increased levels of KLF6, p21, and p27(kip1) in cells transfected with pKLF6 cDNA. pKLF6 cDNA transfected cells showed less compared with control cells in vitro. Conclusions: pKLF6 cDNA inhibited cell proliferation and decreased cell viability of LEC by unregulation of p21 and p27(kip1).

引用

页码：1080 / 1084

页数：5

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