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Archive > Volume 24 Issue 9 > 2017,24(9):960-965. DOI:10.3872/j.issn.1007-385X.2017.09.006 Prev Next
Basic Research
Effect of EZH2 gene on proliferation of human esophageal cancer cells
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Abstract:
Objective: To investigate the effect of EZH2 (enhancer of zeste homolog 2) overexpression or knock-down on the proliferation of esophageal cancer cells. Methods: Human esophageal cancer cell lines ECA109, TE1,KYSE30 and KYSE170 were selected as the research objects. The expression of EZH2 mRNA and protein in esoph-ageal carcinoma cells were detected by Real-time fluorescence quantitative PCR (qPCR) and Western blotting, re-spectively. The mRNA expression of four esophageal cancer cells after overexpression or knockdown of EZH2 was detected by qPCR. The effects of EZH2 overexpression or knockdown as well as EZH2 inhibitor DZNep (3-deazane-planocin A) on the proliferation and clone growth rate of esophageal cancer cells were observed by CCK-8 prolifera-tion assay and clone formation assay. Results: The expression of EZH2 mRNA and protein in ECA109 and TE1 cells was significantly higher than that in KYSE30 and KYSE170 cells (P<0.05). The expression of EZH2 in esoph-ageal cancer TE1 and ECA109 cells was down-regulated after transfection with EZH2-ShRNA, and the cell prolifer-ation was decreased (1.07±0.08 vs 1.59±0.09, P<0.05; 1.05±0.11 vs 0.88±0.08, P<0.05), and the clone formation was also down-regulated (200.00±11.43 vs 480.00±13.10, P<0.05；88.00±8.16 vs 220.00±14.69, P<0.05). The ex-pression of EZH2 was increased in esophageal cancer KYSE30 and KYSE170 cells after transfection of EZH2 over-expression plasmid, and the proliferation ability (1.06±0.07 vs 0.76±0.06, P<0.05；3.36±0.30 vs 1.50±0.08, P<0.05)and clone formation (45.00±3.27 vs 18.00±1.63，P<0.05；65.00±4.08 vs 23.00±2.45，P<0.05) were significantly in-creased. After DZNep treatment, proliferation (all P<0.05) and clone formation (all P<0.05) in ECA109 and TE1 cells were decreased. Conclusion: EZH2 gene can effectively promote the proliferation and cloning ability of esoph-ageal cancer cells, which provides a basis for further study on the mechanism of EZH2 as a target in the treatment of esophageal cancer.
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Project Supported:
Project supported by the Science and Technology Supporting Program of Hebei Prov-ince （No.152777184)
Clc Number:
