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Frontiers of Medicine

ISSN 2095-0217

ISSN 2095-0225(Online)

CN 11-5983/R

Postal Subscription Code 80-967

2018 Impact Factor: 1.847

Front. Med.    2007, Vol. 1 Issue (4) : 390-397     DOI: 10.1007/s11684-007-0076-5
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Effects of galectin-3 inhibition on endometrial cell cycle and adhesion
LEI Caixia1, ZHANG Wei1, SUN Xiaowei1, DU Guoping1, WANG Li1, LIU Yinkun2
1.Laboratory of Reproductive Endocrinology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China; 2.Institution of Liver Cancer, Zhongshan Hospital, Fudan University, Shanghai 200032, China
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Abstract  Galectin-3 (gal-3) and its ligands have been implicated in cell transformation and cancer metastasis. Gal-3 protein has been found in uterine epithelial cells adjacent to implanting blastocysts in different cell types. In order to investigate the role of gal-3 in the establishment of human endometrial receptivity, the expression of gal-3 in human endometrial cell line RL95-2 was silenced by RNA interference technology using gal-3 specific small RNA. The expression of gal-3 was detected by the reverse transcriptase-polymerase chain reaction and Western blot analysis. After the suppression of gal-3, cell cycle changes and the expression of integrin β1 were detected by flow cytometry. The adhesive ability of RL95-2 cells was analyzed by the adhesion test. Gal-3 siRNA transfection efficiency reached 70%–90%. The expression of gal-3 mRNA and protein in RL95-2 cells was strongly inhibited by 70%–90% after RNA interference. Inhibition of gal-3 expression decreased S-phase but increased G1 phase cells. Integrin β1 expression was down-regulated, and the adhesive ability of RL95-2 cells to fibronectin (FN) was significantly reduced. Gal-3 may be involved in the establishment of endometrial receptivity by regulating the proliferation and adhesion of endometrial cells. The influence on adhesion may be related with the integrin modulation.
Issue Date: 05 December 2007
URL:  
http://academic.hep.com.cn/fmd/EN/10.1007/s11684-007-0076-5     OR     http://academic.hep.com.cn/fmd/EN/Y2007/V1/I4/390
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