The type 1 transmembrane glycoprotein B7-H3 interacts with the glycolytic enzyme ENO1 to promote malignancy and glycolysis in HeLa cells

被引：30
|
作者：
Zuo, Jiahui
Wang, Bowen
Long, Min
Gao, Zhaowei
Zhang, Zhe
Wang, Huiping
Wang, Xi
Li, Ruicheng
Dong, Ke [1 ,2 ]
Zhang, Huizhong [1 ,2 ]
机构：
[1] Air Force Med Univ, Affiliated Hosp 2, Dept Med Lab, 569 Xinsi Rd, Xian, Shanxi, Peoples R China
[2] Air Force Med Univ, Affiliated Hosp 2, Res Ctr, 569 Xinsi Rd, Xian, Shanxi, Peoples R China
来源：
FEBS LETTERS | 2018年 / 592卷 / 14期
关键词：
B7-H3; cervical cancer; ENO1; glycolysis; tumor malignancy; ALPHA-ENOLASE; CANCER-CELLS; TUMOR; CARCINOMA; LACTATE; METABOLISM; ACTIVATION; EXPRESSION; TARGET;
D O I：
10.1002/1873-3468.13164
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：
The role of the type 1 transmembrane glycoprotein B7-H3 is controversial in tumorigenesis; thus, a better clarification of its involvement in cancer is crucial. In the present study, 79.3% of cervical cancer samples were found to be B7-H3 positive and the expression of B7-H3 was positively correlated with the clinical features of the samples. Silencing B7-H3 using small interfering RNA or blocking it with intracellular ScFv attenuated the malignancy of HeLa cells. By pull-down assay and liquid chromatography-mass spectrometry in HeLa cells, the glycolytic enzyme ENO1 was found to interact with B7-H3. Subsequently, the involvement of B7-H3 in glycolysis was investigated. We observed decreases in the levels of ATP and lactate, as well as c-Myc and lactate dehydrogenase A, upon B7-H3 downregulation in HeLa cells. The results of the present study provide evidence for B7-H3 mediating tumor glycolysis.
引用
收藏
页码：2476 / 2488
页数：13
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