The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Signaling pathway via TNF-α/NF-κB in intestinal epithelial cells may be directly involved in colitis-associated carcinogenesis
Abstract
Treatment with anti-TNF-α MAb has been accepted as a successful maintenance therapy for patients with inflammatory bowel diseases (IBD). Moreover, it has been recently reported that blockade of TNF receptor (TNFR) 1 signaling in infiltrating hematopoietic cells may prevent the development of colitis-associated cancer (CAC). However, it remains unclear whether the TNF-α signaling in epithelial cells is involved in the development of CAC. To investigate this, we studied the effects of anti-TNF-α MAb in an animal model of CAC by administration of azoxymethane (AOM) followed by sequential dextran sodium sulfate (DSS) ingestion. We observed that the NF-κB pathway is activated in colonic epithelia from DSS-administered mice in association with upregulation of TNFR2 rather than TNFR1. Immunoblot analysis also revealed that the TNFR2 upregulation accompanied by the NF-κB activation is further complicated in CAC tissues induced in AOM/DSS-administered mice compared with the nontumor area. Such NF-κB activity in the epithelial cells is significantly suppressed by the treatment of MP6-XT22, an anti-TNF-α MAb. Despite inability to reduce the severity of colitis, sequential administration of MP6-XT22 reduced the numbers and size of tumors in association with the NF-κB inactivation. Taken together, present studies suggest that the TNFR2 signaling in intestinal epithelial cells may be directly involved in the development of CAC with persistent colitis and imply that the maintenance therapy with anti-TNF-α MAb may prevent the development of CAC in patients with long-standing IBD.
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Cites
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IKKβ Links Inflammation and Tumorigenesis in a Mouse Model of Colitis-Associated Cancer
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Mice deficient in tumor necrosis factor-α are resistant to skin carcinogenesis
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Apoptotic cell death in disease—Current understanding of the NCCD 2023
Vitale, I., Pietrocola, F., Guilbaud, E., Aaronson, S. A., Abrams, J. M., Adam, D., Agostini, M., Agostinis, P., Alnemri, E. S., Altucci, L., et al. (2023) · Cell Death & Differentiation · doi:10.1038/s41418-023-01153-w · Cited by 361
Shin, W., & Kim, H. J. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1810819115 · Cited by 309
Colorectal Cancer in Inflammatory Bowel Disease
Higgins, P., & Stidham, R. (2018) · Clinics in Colon and Rectal Surgery · doi:10.1055/s-0037-1602237 · Cited by 295
Matmati, M., Jacques, P., Maelfait, J., Verheugen, E., Kool, M., Sze, M., Geboes, L., Louagie, E., Guire, C. M., Vereecke, L., et al. (2011) · Nature Genetics · doi:10.1038/ng.874 · Cited by 290
Metadata
- Authors
- Onizawa, M., Nagaishi, T., Kanai, T., Nagano, K.-I., Oshima, S., Nemoto, Y., Yoshioka, A., Totsuka, T., Okamoto, R., Nakamura, T., Sakamoto, N., Tsuchiya, K., Aoki, K., Ohya, K., Yagita, H., & Watanabe, M.
- Venue
- American Journal of Physiology-Gastrointestinal and Liver Physiology
- Publisher
- American Physiological Society
- Published
- 2009-04
- Volume
- 296
- Issue
- 4
- Pages
- G850-G859
- ISSN
- 0193-1857 (ISSN-L)
- 1522-1547
- OpenAlex
- W1985082045
- Cited by
- 163
- References
- 8
- FWCI
- 3.50
- Type
- journal article
- Language
- en
- Open access
- closed
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- Onizawa, M., Nagaishi, T., Kanai, T., Nagano, K.-I., Oshima, S., Nemoto, Y., Yoshioka, A., Totsuka, T., Okamoto, R., Nakamura, T., Sakamoto, N., Tsuchiya, K., Aoki, K., Ohya, K., Yagita, H., & Watanabe, M. (2009). Signaling pathway via TNF-α/NF-κB in intestinal epithelial cells may be directly involved in colitis-associated carcinogenesis. American Journal of Physiology-Gastrointestinal and Liver Physiology. https://doi.org/10.1152/ajpgi.00071.2008
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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