Prostaglandin F2α stimulates motility and invasion in colorectal tumor cells

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Abstract
Increased expression of cyclooxygenase‐2 (COX‐2) and subsequent prostaglandin production is an important event in several human malignancies, including colorectal cancer. COX‐2 mediated prostanoid synthesis has been shown to play a key role in tumor progression with prostaglandin E2 (PGE2) being shown to promote tumor growth, invasion and angiogenesis. The role of the other prostaglandins produced by COX‐2 in tumors remains poorly understood. We have shown that colorectal tumor cells produce prostaglandin F2α (PGF2α) and provide evidence that PGF2α may play an important role in colorectal tumorigenesis. Our data show that PGF2α is secreted by both colorectal adenoma and carcinoma‐derived cell lines at levels in excess of those detected for PGE2. These cell lines were also found to express the PGF2α receptor (FP) indicating potential autocrine effects of PGF2α. This finding is further supported by an in vivo immunohistochemical study of FP expression in resected colon tissue. These data show epithelial expression of FP in normal colorectal mucosa and also in colorectal adenomas and carcinomas. We compared the relative abilities of PGF2α and PGE2 to induce cell motility in vitro in colorectal tumor cell lines and show the first evidence of prostaglandin‐induced cell motility in colorectal adenoma cell lines. PGF2α induced cell motility with equivalent potency to PGE2 in all the cell lines tested and was also shown to increase the invasion of carcinoma‐derived cells into reconstituted basement membrane. These data show that PGF2α may play an important role in the malignant progression of colorectal tumors.

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