High Glucose Promotes Pancreatic Cancer Cell Proliferation via the Induction of EGF Expression and Transactivation of EGFR

被引:111
作者
Han, Liang [1 ]
Ma, Qingyong [1 ]
Li, Junhui [1 ]
Liu, Han [1 ]
Li, Wei [1 ]
Ma, Guodong [1 ]
Xu, Qinhong [1 ]
Zhou, Shuang [2 ]
Wu, Erxi [2 ]
机构
[1] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, Xian 710049, Peoples R China
[2] N Dakota State Univ, Dept Pharmaceut Sci, Fargo, ND 58105 USA
来源
PLOS ONE | 2011年 / 6卷 / 11期
关键词
EPIDERMAL-GROWTH-FACTOR; FACTOR RECEPTOR; KINASE; ACTIVATION; PROTEIN;
D O I
10.1371/journal.pone.0027074
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Multiple lines of evidence suggest that a large portion of pancreatic cancer patients suffer from either hyperglycemia or diabetes, both of which are characterized by high blood glucose level. However, the underlying biological mechanism of this phenomenon is largely unknown. In the present study, we demonstrated that the proliferative ability of two human pancreatic cancer cell lines, BxPC-3 and Panc-1, was upregulated by high glucose in a concentration-dependent manner. Furthermore, the promoting effect of high glucose levels on EGF transcription and secretion but not its receptors in these PC cell lines was detected by using an EGF-neutralizing antibody and RT-PCR. In addition, the EGFR transactivation is induced by high glucose levels in concentration- and time-dependent manners in PC cells in the presence of the EGF-neutralizing antibody. These results suggest that high glucose promotes pancreatic cancer cell proliferation via the induction of EGF expression and transactivation of EGFR. Our findings may provide new insight on the links between high glucose level and PC in terms of the molecular mechanism and reveal a novel therapeutic strategy for PC patients who simultaneously suffer from either diabetes or hyperglycemia.
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页数:7
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