Octreotide induces apoptosis in the oxyntic mucosa

被引：6

作者：

Erlandsen, Sten Even

Fykse, Vidar

Waldum, Helge L.

Sandvik, Ame K. ^{[1
]}

机构：

[1] Norwegian Univ Sci & Technol, Dept Canc Res & Mol Med, NO-7489 Trondheim, Norway

[2] Univ Trondheim, St Olavs Hosp, Dept Med, Trondheim, Norway

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2007年 / 264卷 / 1-2期

关键词：

regulation; proliferation; affymetrix GeneChip; qRT-PCR; immunohistochemistry;

D O I：

10.1016/j.mce.2006.12.031

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Previous studies show that octreotide LAR causes regression of gastric ECL-cell carcinoids, reducing both number and size of tumours. This study examines the molecular mechanisms behind the antiproliferative effect of octreotide on the oxyntic mucosa. Female rats received octreotide LAR for 21 days. Serum gastrin was measured and tissue samples for RNA extraction and histology collected from the oxyntic mucosa. Affymetrix analysis showed regulated genes related to apoptosis and proliferation, and a large group of regulated growth-related transcription factors. Verification by real time qRT-PCR showed a high degree of consistency to the microarray results. Supporting the molecular results, histomorphometry showed significant decreases in the number of gastric glands, cells per gland and length of glands, and a tendency towards increased apoptosis and decreased proliferation. Thus, octreotide exerts a negative effect on oxyntic mucosal growth, and induces extensive gene expression changes relevant to growth regulation. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

引用

页码：188 / 196

页数：9

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[41] Prolactin (PRL)-PRL receptor system increases cell proliferation involving JNK (c-jun amino terminal kinase) and AP-1 activation: Inhibition by glucocorticoids [J].