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Modeling Colitis-Associated Cancer with Azoxymethane (AOM) and Dextran Sulfate Sodium (DSS)
Published on: September 11, 2012
Zeaxanthin Suppresses Azoxymethane/Dextran Sodium Sulfate-Induced Colorectal Cancer in Mice by Inhibiting
Mengxiang Yang1, Yuejun Han1, Ting Jin2
1Department of Colorectal Surgery, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Zhejiang, China.
Background/Aims:
The treatment of colorectal cancer (CRC) remains a challenge in clinical research. Zeaxanthin (ZEA) has demonstrated substantial anti-inflammatory and anticancer effects. However, its preventive effects and underlying mechanisms in CRC remain elusive. Therefore, this study investigated the preventive effects and 10 molecular mechanisms of ZEA in CRC.
Materials And Methods:
The effects of ZEA on tumor formation, inflammatory responses, and cell proliferation were investigated in an azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced mouse model of CRC. Furthermore, the anti-inflammatory and antiproliferative mechanisms of ZEA were evaluated in vitro using lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and CRC cell lines (HCT116 and SW620).
Results:
Treatment with 50 mg/kg ZEA significantly inhibited AOM/DSS-induced CRC progression. Furthermore, treatment with ZEA reduced tumor formation in the colonic lining, increased body weight, enhanced colorectal length, improved overall survival rate, and attenuated pathological changes in mice. Moreover, ZEA significantly reduced proinflammatory cytokines (tumor necrosis factor-α and interleukin-1β) and Ki-67 expression levels. Mechanistically, ZEA mitigated inflammation in LPS-stimulated RAW264.7 macrophages by suppressing the nucleotide-binding oligomerization domain-containing protein 1 (NOD1)/receptor-interacting protein 2 kinase (RIP2)/ nuclear factor-κB (NF-κB) signaling pathway. In addition, it suppressed proliferation of HCT116 and SW620 cells by inhibiting the signaling pathway of PI3K/AKT/MYC.
Conclusion:
ZEA exerted significant anti-CRC effects, including anti-inflammatory and antiproliferative actions through multitarget mechanisms, such as modulation of the NOD1/RIP2/NF-κB and PI3K/AKT/MYC signaling pathways. These findings suggest that ZEA is a promising natural chemopreventive agent for the prevention and treatment of CRC.
Insights
Zeaxanthin (ZEA) shows significant preventive effects against colorectal cancer (CRC) by reducing inflammation and cell proliferation. This natural compound modulates key signaling pathways, suggesting its potential as a chemopreventive agent for CRC.
Area of Science:
- Oncology
- Molecular Biology
- Natural Product Chemistry
Background:
- Colorectal cancer (CRC) treatment presents ongoing clinical challenges.
- Zeaxanthin (ZEA) exhibits known anti-inflammatory and anticancer properties.
- Preventive effects and mechanisms of ZEA in CRC require further elucidation.
Purpose of the Study:
- To investigate the preventive efficacy of Zeaxanthin (ZEA) in colorectal cancer (CRC).
- To elucidate the molecular mechanisms underlying ZEA's chemopreventive actions in CRC.
Main Methods:
- Utilized an azoxymethane (AOM)/dextran sodium sulfate (DSS) induced mouse model for CRC.
- Assessed ZEA's effects on tumor formation, inflammation, and proliferation in vivo.
- Evaluated anti-inflammatory and anti-proliferative mechanisms in vitro using RAW264.7 macrophages and CRC cell lines (HCT116, SW620).
Main Results:
- ZEA (50 mg/kg) significantly inhibited CRC progression, reduced tumor formation, and improved survival rates in mice.
- ZEA treatment decreased pro-inflammatory cytokines (TNF-α, IL-1β) and Ki-67 expression.
- ZEA suppressed inflammation via the NOD1/RIP2/NF-κB pathway and proliferation via the PI3K/AKT/MYC pathway in vitro.
Conclusions:
- Zeaxanthin (ZEA) demonstrates significant anti-CRC effects through anti-inflammatory and anti-proliferative actions.
- ZEA targets multiple molecular pathways, including NOD1/RIP2/NF-κB and PI3K/AKT/MYC.
- ZEA shows promise as a natural chemopreventive agent for colorectal cancer prevention and treatment.
