ArticleDigestive diseases and sciences2008
The COX-2 selective inhibitor-independent COX-2 effect on colon carcinoma cells is associated with the Delta1/Notch1 pathway.
Article in Digestive diseases and sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 25 citations in OpenAlex.
- Notch receptor/ligand diversity: contribution to colorectal cancer stem cell heterogeneity.Frontiers in cell and developmental biology · 2023Review
- NS398 as a potential drug for autosomal-dominant polycystic kidney disease: Analysis using bioinformatics, and zebrafish and mouse models.Journal of cellular and molecular medicine · 2021Article
- Curcumin attenuates hypoxia/reoxygenation‑induced cardiomyocyte injury by downregulating Notch signaling.Molecular medicine reports · 2019Article
- Computational Model for Predicting the Relationship Between Micro-RNAs and Their Target Messenger RNAs in Breast and Colon Cancers.Cancer informatics · 2018Article
- Modulators affecting the immune dialogue between human immune and colon cancer cells.World journal of gastrointestinal oncology · 2014Review
- Chemopreventive drugs: mechanisms via inhibition of cancer stem cells in colorectal cancer.World journal of gastroenterology · 2014Review
- Ibuprofen inhibits colitis-induced overexpression of tumor-related Rac1b.Neoplasia (New York, N.Y.) · 2013Article
- The effects of piroxicam and deracoxib on canine mammary tumour cell line.TheScientificWorldJournal · 2012Article
- Role of Notch and its oncogenic signaling crosstalk in breast cancer.Biochimica et biophysica acta · 2011Review
- NOTCH signaling is required for formation and self-renewal of tumor-initiating cells and for repression of secretory cell differentiation in colon cancer.Cancer research · 2010Article
- Enhancement of 5-fluorouracil efficacy on high COX-2 expressing HCA-7 cells by low dose indomethacin and NS-398 but not on low COX-2 expressing HT-29 cells.Pathology oncology research : POR · 2009Article
- In vivo optical molecular imaging of matrix metalloproteinase activity following celecoxib therapy for colorectal cancer.Molecular imagingArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCyclooxygenase-2 (COX-2) is a key factor in the development of colorectal cancer, and non-steroidal anti-inflammatory drugs (NSAIDs) have anti-colorectal cancer activity. However, the potential molecular mechanism of the COX-2 selective inhibitor effect on proliferation and apoptosis of colon cancer cells is unclear. In this study, we have demonstrated for the first time that the Delta1/Notch1 signal transduction pathway mediates the COX-2 selective inhibitor effect on colorectal cancer cells, and we reveal the mechanism of the Notch1 pathway in terms of regulating the proliferation and apoptosis of colorectal cancer cells. METHODS AND
resultColon cancer cell lines HT-29 and SW480 were treated with NS-398 (a COX-2 selective inhibitor) and DAPT (a gamma-secretase inhibitor). The colormetric MTT cell proliferation assay and flow cytometry were used to measure cell proliferation and apoptosis. Reverse transcriptase (RT)-PCR and ELISA analyses were used to detect the levels of COX-2 mRNA expression and prostaglandin E2 (PGE2) concentration from the two cell lines, respectively. The expression of the Notch1, Delta1, ICN, Hes1 and NF-kappaB2 proteins was measured by Western blot. Immunohistochemistry results showed that Notch1 was expressed mainly in the cytoplasm and ICN mainly in the nucleus. COX-2 mRNA was highly expressed in HT-29 cells but not in SW480 cells. Both COX-2 mRNA expression and PGE2 concentration decreased in HT-29 cells treated with NS-398; however, PGE2 levels did not change in SW480 cells treated with NS-398. NS-398 and DAPT inhibited cell proliferation and induced apoptosis in a dose time-dependent manner accompanied by significantly decreased Notch1 activity (P < 0.01), and resulted in a significant down-regulation of Hes1 and NF-kappaB2 (P < 0.01).
conclusionsOur results show that the selective COX-2 inhibitor may inhibit the proliferation and induce apoptosis in colon cancer cells through the COX-2-dependent pathway (HT-29) by decreasing the COX-2 mRNA/PGE2 levels and the activity of the COX-2-independent pathway (SW480). The Notch1 signal pathway mediates the effects of the COX-2 inhibitor on the proliferation and apoptosis of colon cancer cells. This may be a new target of the selective COX-2 inhibitor effect on colon cancer.
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