Sodium salicylate and 5-aminosalicylic acid synergistically inhibit the growth of human colon cancer cells and mouse intestinal polyp-derived cells
Copyright © 2022 JCBN..
As colon cancer is one of the most common cancers in the world, practical prevention strategies for colon cancer are needed. Recently, treatment with aspirin and/or 5-aminosalicylic acid-related agents was reported to reduce the number of intestinal polyps in patients with familial adenomatous polyposis. To evaluate the mechanism of aspirin and 5-aminosalicylic acid for suppressing the colon polyp growth, single and combined effects of 5-aminosalicylic acid and sodium salicylate (metabolite of aspirin) were tested in the two human colon cancer cells with different cyclooxygenase-2 expression levels and intestinal polyp-derived cells from familial adenomatous polyposis model mouse. The combination induced cell-cycle arrest at the G1 phase along with inhibition of cell growth and colony-forming ability in these cells. The combination reduced cyclin D1 via proteasomal degradation and activated retinoblastoma protein. The combination inhibited the colony-forming ability of mouse colonic mucosa cells by about 50% and the colony-forming ability of mouse intestinal polyp-derived cells by about 90%. The expression level of cyclin D1 in colon mucosa cells was lower than that in intestinal polyp-derived cells. These results suggest that this combination may be more effective in inhibiting cell growth of intestinal polyps through cyclin D1 down-regulation.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2022 |
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Erschienen: |
2022 |
Enthalten in: |
Zur Gesamtaufnahme - volume:70 |
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Enthalten in: |
Journal of clinical biochemistry and nutrition - 70(2022), 2 vom: 04. März, Seite 93-102 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Takakura, Hideki [VerfasserIn] |
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Links: |
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Themen: |
Aspirin |
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Anmerkungen: |
Date Revised 13.04.2022 published: Print-Electronic Citation Status PubMed-not-MEDLINE |
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doi: |
10.3164/jcbn.21-74 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM33930457X |
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520 | |a As colon cancer is one of the most common cancers in the world, practical prevention strategies for colon cancer are needed. Recently, treatment with aspirin and/or 5-aminosalicylic acid-related agents was reported to reduce the number of intestinal polyps in patients with familial adenomatous polyposis. To evaluate the mechanism of aspirin and 5-aminosalicylic acid for suppressing the colon polyp growth, single and combined effects of 5-aminosalicylic acid and sodium salicylate (metabolite of aspirin) were tested in the two human colon cancer cells with different cyclooxygenase-2 expression levels and intestinal polyp-derived cells from familial adenomatous polyposis model mouse. The combination induced cell-cycle arrest at the G1 phase along with inhibition of cell growth and colony-forming ability in these cells. The combination reduced cyclin D1 via proteasomal degradation and activated retinoblastoma protein. The combination inhibited the colony-forming ability of mouse colonic mucosa cells by about 50% and the colony-forming ability of mouse intestinal polyp-derived cells by about 90%. The expression level of cyclin D1 in colon mucosa cells was lower than that in intestinal polyp-derived cells. These results suggest that this combination may be more effective in inhibiting cell growth of intestinal polyps through cyclin D1 down-regulation | ||
650 | 4 | |a Journal Article | |
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700 | 1 | |a Horinaka, Mano |e verfasserin |4 aut | |
700 | 1 | |a Imai, Ayaka |e verfasserin |4 aut | |
700 | 1 | |a Aono, Yuichi |e verfasserin |4 aut | |
700 | 1 | |a Nakao, Toshimasa |e verfasserin |4 aut | |
700 | 1 | |a Miyamoto, Shingo |e verfasserin |4 aut | |
700 | 1 | |a Iizumi, Yosuke |e verfasserin |4 aut | |
700 | 1 | |a Watanabe, Motoki |e verfasserin |4 aut | |
700 | 1 | |a Narita, Takumi |e verfasserin |4 aut | |
700 | 1 | |a Ishikawa, Hideki |e verfasserin |4 aut | |
700 | 1 | |a Mutoh, Michihiro |e verfasserin |4 aut | |
700 | 1 | |a Sakai, Toshiyuki |e verfasserin |4 aut | |
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