FHIT is up-regulated by inflammatory stimuli and inhibits prostaglandin E2-mediated cancer progression

Cancer Research
Koshi MimoriMasaki Mori

Abstract

The FHIT gene is known to be susceptible to environmental carcinogens. Formation of prostaglandin E(2) (PGE(2)) is catalyzed by cyclooxygenase-2 (COX-2) and may influence malignant phenotype in colorectal cancer. We explored whether FHIT might play a role in progression of colorectal cancer through inflammation-associated PGE(2) activity. Immunohistochemical study of COX-2 and FHIT expression was done in 92 colorectal cancer tumors. We also used a FHIT-expressing cancer cell line (H460) induced by ponasterone A and two FHIT small interfering RNA-treated colorectal cancer cell lines (CCK81 and DLD1). After PGE(2) stimulation, we compared synthesis of PGE(2) (ELISA assay) and cell proliferation [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay]. Immunohistochemistry showed a significant association between COX-2 and FHIT expression in colorectal cancers (P < 0.01). In a subset of 41 COX-2-expressing tumors, 12 FHIT(-) tumors showed deeper cancer invasion than 29 FHIT(+) tumors (P < 0.01). Experimental study, however, showed there was no direct interaction between FHIT and COX-2. Considered with results from another experiment with epidermal growth factor receptor (EGFR), we hypothesize that FHIT and COX-2 might ...Continue Reading

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Citations

Dec 8, 2006·Annals of Surgical Oncology·Koshi MimoriMasaki Mori
Mar 28, 2012·The Journal of Pathology·Irene RomeroAngel M Garcia-Lora
Sep 25, 2012·Cellular Signalling·Fereshteh Mir MohammadrezaeiMohammad Hossein Ghahremani
Jun 26, 2013·The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society·Rabeah Abbas Al-TemaimiFahd Al-Mulla

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