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Updated: Aug 22, 2026
Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue
Published on: October 12, 2013
Subepithelial myofibroblasts express cyclooxygenase-2 in colorectal tubular adenomas
Patrick A Adegboyega1, Omiyosoye Ololade, Jamal Saada
1Department of Pathology, 2190 John Sealy Annex, Mail Route 0588, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0588, USA. paadegbo@utmb.edu
Purpose:
Recent data support the hypothesis that the inducible isoform of cyclooxygenase (COX-2) plays a role in the early stages of colonic carcinogenesis and that nonsteroidal anti-inflammatory drugs (NSAIDs) retard the development of colon cancer by modulating COX-2. However, the cell types responsible for producing COX-2 in colorectal adenomas remain a subject of controversy.
Experimental Design:
COX-2 expression in normal colonic mucosa (n = 50), hyperplastic polyps (n = 43), sporadic adenomas (n = 67), and invasive colonic adenocarcinoma (n = 39) was studied in formalin-fixed and paraffin-embedded tissue sections from endoscopy biopsy and colonic resection specimens. Immunohistochemistry (avidin-biotin complex technique with double immunolabeling) was used to identify the phenotypes of COX-2-producing cells.
Results:
In colorectal adenomas, increased expression of COX-2 was detected and localized to alpha smooth muscle actin ( proportional, variant SMA)-positive subepithelial stromal cells (myofibroblasts) in the periluminal region of the lamina propria in 63 (94%) of 67 cases. In contrast, in normal colonic mucosa and in hyperplastic polyps with intact epithelium, COX-2 expression was found only in macrophages and endothelial cells. In areas in which the surface epithelium was ulcerated in normal mucosa as well as hyperplastic or neoplastic polyps, COX-2 expression was increased in granulation tissue (and present in macrophages, endothelium, and myofibroblasts). In invasive carcinoma, COX-2 expression in myofibroblasts was limited to the adenomatous portion of the tumor and was detected in 62% of cases (n = 39). In addition, focal expression of COX-2 by malignant epithelial cells was observed in 23% of invasive adenocarcinoma.
Conclusions:
These results show that increased COX-2 expression in sporadic adenoma of the colon is common and is localized specifically to subepithelial intestinal myofibroblasts. These findings further support the hypothesis that myofibroblasts are important target cells for NSAID-mediated chemoprevention of colorectal cancer.
Insights
Colorectal adenomas commonly show increased cyclooxygenase-2 (COX-2) expression, specifically in subepithelial myofibroblasts. This finding supports myofibroblasts as key targets for nonsteroidal anti-inflammatory drug (NSAID) cancer prevention.
Area of Science:
- Gastroenterology
- Oncology
- Molecular Biology
Background:
- Cyclooxygenase-2 (COX-2) is implicated in early colonic carcinogenesis.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) may prevent colon cancer by modulating COX-2.
- The specific cell types expressing COX-2 in colorectal adenomas are not fully understood.
Purpose of the Study:
- To investigate the cellular localization of COX-2 expression in colorectal adenomas.
- To identify the cell types responsible for COX-2 production in the progression of colorectal neoplasia.
Main Methods:
- Immunohistochemistry was used to detect COX-2 expression in formalin-fixed, paraffin-embedded tissues.
- Tissues analyzed included normal colonic mucosa, hyperplastic polyps, sporadic adenomas, and invasive adenocarcinomas.
- Double immunolabeling identified the phenotypes of COX-2-producing cells.
Main Results:
- Increased COX-2 expression was found in 63% of colorectal adenomas, localized to alpha smooth muscle actin-positive subepithelial myofibroblasts.
- In normal mucosa and hyperplastic polyps, COX-2 was mainly in macrophages and endothelial cells.
- Ulcerated areas showed increased COX-2 in granulation tissue, including myofibroblasts.
Conclusions:
- Increased COX-2 expression is common in sporadic colorectal adenomas and specifically located in subepithelial intestinal myofibroblasts.
- These findings highlight myofibroblasts as crucial target cells for NSAID-mediated chemoprevention of colorectal cancer.
