Prostaglandin E2 Increases Growth and Motility of Colorectal Carcinoma Cells*
By H. Sheng, J. Shao, M. Washington, R. Dubois. Journal of Biological Chemistry, 2001
689 citations recorded by the source corpus.
Chronic use of nonsteroidal anti-inflammatory drugs results in a significant reduction of risk and mortality from colorectal cancer in humans. All of the mechanism(s) by which nonsteroidal anti-inflammatory drugs exert their protective effects are not completely understood, but they are known to inhibit cyclooxygenase activity. The cyclooxygenase enzymes catalyze a key reaction in the conversion of arachidonic acid to prostaglandins, such as prostaglandin E2 (PGE2). Here we demonstrate that PGE2 treatment of LS-174 human colorectal carcinoma cells leads to increased motility and changes in cell shape. The prostaglandin EP4 receptor signaling pathway appears to play a role in transducing signals which regulate these effects. PGE2 treatment results in an activation of phosphatidylinositol 3-kinase/protein kinase B pathway that is required for the PGE2-induced changes in carcinoma cell motility and colony morphology. Our results suggest that PGE2 might enhance the invasive potential of colorectal carcinoma cells via activation of major intracellular signal transduction pathways not previously reported to be regulated by prostaglandins.
Subfields: Genetics, Molecular Biology, Pharmacology
View Paper: https://www.semanticscholar.org/paper/d4a61fe30f51d0c1f6f8b3f46cbf900fe1b34f04
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Citations in the corpus
- Prostaglandin E2 transactivates EGF receptor: A novel mechanism for promoting colon cancer growth and gastrointestinal hypertrophy (2002, background): “gif" NDATA ITEM> ]> Physiological functions of prostaglandins (PGs) in the gastrointestinal tract include inhibiting gastric-acid secretion, stimulating bicarbonate and mucus secretion, maintaining mucosal integrity and increasing DNA synthesi”
- Cyclooxygenase Isozymes: The Biology of Prostaglandin Synthesis and Inhibition (2004, background): “In addition, epithelial cell motility and invasive behavior were also induced (Sheng et al., 2001).”
- The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment. (2009, background): “Further studies have demonstrated that PGE2 promotes cytoskeletal reorganisation and increases colorectal cancer cell migration and invasion via PI3K signalling [67].”
- IL‐1β mediated up‐regulation of HIF‐lα via an NFkB/COX‐2 pathway identifies HIF‐1 as a critical link between inflammation and oncogenesis (2003, background): “Furthermore, the COX-2 gene product PGE2 has also been shown to be a major contributor of carcinogenesis (69, 70).”