High glucose promotes pancreatic cancer cell proliferation via the induction of EGF expression and transactivation of EGFR.
High glucose promotes pancreatic cancer cell proliferation via the induction of EGF expression and transactivation of EGFR.
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高血糖通过诱导 EGF 表达和 EGFR 反式激活促进胰腺癌细胞增殖
DOI:
10.1371/journal.pone.0027074
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发表时间:
2011
期刊:
影响因子:
3.7
通讯作者:
Wu E
中科院分区:
文献类型:
--
作者:
Han L;Ma Q;Li J;Liu H;Li W;Ma G;Xu Q;Zhou S;Wu E
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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影响因子:
3.7
作者:
Li J;Ma Q;Liu H;Guo K;Li F;Li W;Han L;Wang F;Wu E
通讯作者:
Wu E
影响因子:
9.7
作者:
Lee, EunAh;Yi, Jae Youn;Son, Youngsook
通讯作者:
Son, Youngsook
DOI:
10.1152/ajprenal.00159.2001
发表时间:
2002-04-01
影响因子:
4.2
作者:
Gekle, M;Freudinger, R;Silbernagl, S
通讯作者:
Silbernagl, S
影响因子:
4.8
作者:
Soltoff, SP;Cantley, LC
通讯作者:
Cantley, LC
影响因子:
64.5
作者:
Hsu, Peggy P.;Sabatini, David M.
通讯作者:
Sabatini, David M.