Function and mechanism of zinc finger protein ZNF50 in inhibiting the growth of esophageal squamous cell carcinoma cells

Juan Wang; Yanghui BI; Jie Yang; Feng Liu; Yike LI; Heyang Cui; Fang Wang; Jing Liu; Bin Yang; Ling Zhang

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Function and mechanism of zinc finger protein ZNF50 in inhibiting the growth of esophageal squamous cell carcinoma cells

VernacularTitle: 锌指蛋白750在抑制食管鳞癌细胞生长中的作用及相关机制
Author: Juan WANG ¹ ; Yanghui BI ¹ ; Jie YANG ¹ ; Feng LIU ² ; Yike LI ¹ ; Heyang CUI ¹ ; Fang WANG ¹ ; Jing LIU ³ ; Bin YANG ⁴ ; Ling ZHANG ⁵
Author Information

1. Translational Medicine Research Center, Shanxi Medical University, Taiyuan 030001, China
2. Department of Material Evidence, College of Forensic Medicine, Shanxi Medical University, Taiyuan 030001, China
3. Department of General Surgery, The First Affiliated Hospital, Shanxi Medical University, Taiyuan 030001, China
4. Department of Thoracic Surgery, Shanxi Cancer Hospital, Taiyuan 030013, China
5. Department of Pathology, College of Preclinical Medicine, Shanxi Medical University, Taiyuan 030001, China
Publication Type:Journal Article
Keywords: Esophageal neoplasms; Carcinoma, squamous cell; Genome-wide association study; Zinc finger protein 750; Kruppel-like factor 4
From: Chinese Journal of Oncology 2017;39(1):7-12
CountryChina
Language:Chinese
Abstract: Objective:To investigate the function and mechanism of zinc finger protein 750 (ZNF750) in esophageal squamous cell carcinoma (ESCC).
Methods:Xenograft in nude mice was applied to detect the tumorigenesis of ZNF750-depleted ESCC cells. Western blot was performed to observe the expression of downstream target protein of ZNF750 in ESCC cell lines and xenograft tumor tissues in which ZNF750 was knocked down. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assay was used to determine the proliferation of ZNF750 stably depleted cells after restoration of its target protein.
Results:The tumor weight of blank control, negative control and ZNF750 knockdown groups was 137±26 mg, 161±31 mg and 463±89 mg, respectively, with a statistically significant difference (P<0.01). The expressions of Kruppel-like factor 4 (KLF4) in ZNF750-depleted ESCC cells and its derived tumor tissue xenograft in nude mice were significantly down-regulated. Restoration of KLF4 in ZNF750 stably depleted cells significantly inhibited the cell proliferation (P<0.01).
Conclusions:ZNF750 may be a new tumor suppressor in the tumorigenesis of ESCC, and the inhibition of cell proliferation induced by ZNF750 may be partially through the regulation of KLF4 expression.