Cholecystokinin mediates progression and metastasis of pancreatic cancer associated with dietary fat.
Cholecystokinin mediates progression and metastasis of pancreatic cancer associated with dietary fat.
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DOI：
10.1007/s10620-014-3201-8
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发表时间：
2014-06
影响因子：
3.1
通讯作者：
Smith, Jill P.
中科院分区：
文献类型：
--
作者：
Matters, Gail L.;Cooper, Timothy K.;McGovern, Christopher O.;Gilius, Evan L.;Liao, Jiangang;Barth, Brian M.;Kester, Mark;Smith, Jill P.
Obesity and dietary fat are associated with increased risk of several malignancies including pancreatic cancer. The incidence of pancreatic cancer is increased in countries that consume diets high in fat. The purpose of this study was to assess the relationship and mechanism of action between dietary fat and endogenous cholecystokinin (CCK) on pancreatic tumor growth and metastasis in an immunocompetent animal model. C57BL/6 mice were placed on regular, low-fat, or high-fat diets for 8 weeks before establishment of Panc-02 orthotopic pancreatic tumors. Mice were then treated with a CCK-A receptor antagonist, devazepide, or vehicle for an additional 2.5 weeks. Pancreas tumors were weighed and metastases counted. Blood CCK levels were measured by radioimmunoassay (RIA). Tissues were examined histologically and studied for genes associated with metastasis by RT-PCR array. Effects of the CCK antagonist on Panc-02 cells invasiveness was assessed in a Matrigel invasion assay. Mice that received the high-fat diet had larger tumors and tenfold higher serum CCK levels by RIA compared to normal diet controls (p < 0.01). Pancreatic tumors in high-fat diet mice treated with the antagonist had fewer intravascular tumor emboli and metastases compared to controls. The reduction in tumor emboli correlated with decreased vascular endothelial growth factor-A (VEGF-A) expression in tumors (p < 6 × 10−9). In vitro invasiveness of Panc-02 cells also was reduced by CCK-A receptor antagonist treatment (p = 1.33 × 10−6). CCK is a mediator of dietary fat-associated pancreatic cancer. CCK is also involved in the invasiveness of pancreatic tumors through a mechanism involving VEGF-A.
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DOI：
10.1158/1940-6207.capr-13-0065
发表时间：
2013-10
期刊：
Cancer prevention research (Philadelphia, Pa.)
影响因子：
--
作者：
Dawson DW;Hertzer K;Moro A;Donald G;Chang HH;Go VL;Pandol SJ;Lugea A;Gukovskaya AS;Li G;Hines OJ;Rozengurt E;Eibl G
通讯作者：
Eibl G
影响因子：
29.4
作者：
Alemán JO;Eusebi LH;Ricciardiello L;Patidar K;Sanyal AJ;Holt PR
通讯作者：
Holt PR
饮食能量平衡的调节kras和ink4a/arf+/ - 驱动胰腺癌：胰岛素样生长因子I的作用。
DOI：
10.1158/1940-6207.capr-13-0185
发表时间：
2013-10
期刊：
Cancer prevention research (Philadelphia, Pa.)
影响因子：
--
作者：
Lashinger LM;Harrison LM;Rasmussen AJ;Logsdon CD;Fischer SM;McArthur MJ;Hursting SD
通讯作者：
Hursting SD
影响因子：
37.3
作者：
Korc, M
通讯作者：
Korc, M
影响因子：
254.7
作者：
Siegel, Rebecca;Naishadham, Deepa;Jemal, Ahmedin
通讯作者：
Jemal, Ahmedin