Prostaglandin E2 stimulates the growth of colon cancer cells via induction of amphiregulin.

نویسندگان

  • Jinyi Shao
  • Sean B Lee
  • Huiping Guo
  • B Mark Evers
  • Hongmiao Sheng
چکیده

Prostaglandin E(2) (PGE(2)), a major product of cyclooxygenase enzymes, is implicated in colorectal carcinogenesis and has been shown to stimulate the growth of human colorectal carcinoma cells. Here, we show that PGE(2) activated the cyclic AMP/protein kinase A pathway, which induced the expression of amphiregulin (AR), an epidermal growth factor family member, through activation of a cyclic AMP-responsive element in the AR promoter. AR exerted a mitogenic effect on LS-174 cells and partially mediated the PGE(2)-induced growth stimulation. In addition, PGE(2), in collaboration with transforming growth factor-alpha or K-Ras oncogene, synergistically induced AR expression and activated receptor tyrosine kinase-dependent signaling pathways. Our results provide novel mechanisms for cyclooxygenase-2 pro-oncogenic activity and suggest that PGE(2) may act with major oncogenic pathways in a synergistic fashion to activate the epidermal growth factor receptor signaling system through a ligand-dependent autocrine pathway.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Both stromal cell and colonocyte epidermal growth factor receptors control HCT116 colon cancer cell growth in tumor xenografts.

Colon cancer growth requires growth-promoting interactions between malignant colonocytes and stromal cells. Epidermal growth factor receptors (EGFR) are expressed on colonocytes and many stromal cells. Furthermore, EGFR is required for efficient tumorigenesis in experimental colon cancer models. To dissect the cell-specific role of EGFR, we manipulated receptor function on stromal cells and can...

متن کامل

Vascular endothelial growth factor gene expression in colon cancer cells exposed to prostaglandin E2 is mediated by hypoxia-inducible factor 1.

Prostaglandin E(2) (PGE(2)) has been implicated as an inducer of angiogenesis in human colon cancer. Here, we demonstrate that PGE(2) exposure induces the expression of vascular endothelial growth factor (VEGF) mRNA in HCT116 human colon carcinoma cells that is mediated by the transcriptional activator hypoxia-inducible factor 1 (HIF-1). PGE(2) exposure induces the phosphorylation of extracellu...

متن کامل

Investigation of the Effect of Lactobacillus Brevis Bacteria on the Expression of Rel A, IKB, and Casp3 Genes in HT29 Colon Cancer Cells

Aims Studies have shown that probiotic bacteria inhibit the onset and progression of carcinogenesis through different pathways. Our objective in this study was to determine the effect of probiotic bacteria on the expression of growth-related genes Rel A, IKB, and Casp3 in HT29 colon cancer cells Methods & Materials In this study, the Lactobacillus brevis probiotic bacteria were first cultured,...

متن کامل

The Study of the Effects of Acetobacter Isolated from Local Picklesin PTEN/AKT Signaling Route in Colon Cancer Cells (HT29)

Introduction: The imbalance of the microbial ecosystem causes biological changes associated with colorectal cancer and cell proliferation and their planned death, as well as the immune responses. The aim of this study was to determine the effect of probiotic bacteria on the expression of genes associated with growth, metastasis and apoptosis in cancer cells of the HT29 colon.   Materials & Me...

متن کامل

Invasiveness of Cancer Cells by Heregulin and Prostaglandin A Three-Dimensional and Temporo-Spatial Model to Study

To study the temporal expression of motile structures and protease activity during colon cancer cell invasion by heregulin-b1 (HRG) and prostaglandin E2 (PGE2), we have developed a three-dimensional spatial model system. HRG and PGE2 each induced the formation of wellorganized, three-dimensional structures with empty spaces in the center and stimulated the expression of urokinase plasminogen ac...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Cancer research

دوره 63 17  شماره 

صفحات  -

تاریخ انتشار 2003