J Biol Chem 2001,276(21):18075–18081 PubMedCrossRef

J Biol Chem 2001,276(21):18075–18081.PubMedCrossRef

Oligomycin A mouse 12. Chuang PC, Sun HS, Chen TM, Tsai SJ: Prostaglandin E2 induces fibroblast growth factor 9 via EP3-dependent protein kinase Cdelta and Elk-1 signaling. Mol Cell Biol 2006,26(22):8281–8292.PubMedCrossRef 13. Shao J, Lee SB, Guo H, Evers BM, Sheng H: Prostaglandin E2 stimulates the growth of colon cancer cells via induction of amphiregulin. Cancer Res 2003,63(17):5218–5223.PubMed 14. Ding YB, Shi RH, Tong JD, Li XY, Zhang GX, Xiao WM, Yang JG, Bao Y, Wu J, Yan ZG, Wang XH: PGE2 up-regulates vascular endothelial growth factor expression in MKN28 gastric cancer cells via epidermal growth factor receptor signaling system. Exp Oncol 2005,27(2):108–113.PubMed 15. Boyle P, Langman JS: ABC of colorectal cancer: Epidemiology. BMJ 2000,321(7264):805–808.PubMedCrossRef 16. Sheng H, Shao J, Washington MK, DuBois RN: Prostaglandin E2 increases growth and motility of colorectal carcinoma cells. J Biol Chem 2001, 276:18075–18081.PubMedCrossRef 17. Buchanan FG, Wang D, Bargiacchi F, DuBois RN: Prostaglandin E2 regulates cell migration via the intracellular activation of the epidermal

growth factor receptor. J Biol Chem 2003,278(37):35451–7. (2003)PubMedCrossRef Competing interests The authors declare ABT-263 ic50 that they have no competing interests. Authors’ contributions GL performed the experimental programme descried herein. He also prepared the manuscript. PMM acted as clinical liaison on this study and ensured the study was clinically relevant. He also read and proofed the finalised manuscript. PPD acted as a scientific liaison on this study find more and

contributed to the experimental design. He also proofed the finalised manuscript. DWM conceived, designed and trouble-shooted the experimental programme described herein, he acted as a laboratory Linsitinib supervisor to GL and assisted in the preparation and proofing of this manuscript. All authors have read and approved the final manuscript.”
“Introduction A gap junction is a specialized intercellular connection that directly connects the cytoplasm of two cells, and allows various molecules and ions ( < 1 kDa) to pass freely between cells. Gap junctional intercellular communication (GJIC) mediated by gap junctions play an important role in regulating homeostasis, proliferation and differentiation [1, 2]. Gap junction channels contain two hemichannels that are primarily homo -or hetero-hexamers of connexin (Cx) proteins [3]. Twenty types of Cx have been identified as transmembrane proteins [4]. A reduction or loss of GJIC function associated with human carcinomas such as skin cancer, lung cancer, gastric cancer, hepatocellular carcinoma, glioma and prostate cancer, is usually induced by down-regulation of Cxs [5–9]. Moreover, restoration of GJIC in tumor cell lines by Cx transfection can reduce growth and tumorigenicity [10, 11].

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