Loss of transgelin in repeated bouts of ulcerative colitis-induced colon carcinogenesis

Marie Yeo, Dong Kyu Kim, Hee Jin Park, Tae Young Oh, Jang Hee Kim, Sung Won Cho, Young Ki Paik, Ki Baik Nahm

Research output: Contribution to journalArticlepeer-review

36 Citations (Scopus)


Though ulcerative colitis (UC)-associated colon cancer develops from dysplastic lesions caused by chronic inflammation, the specific mechanistic link between chronic inflammation and carcinogenesis in colon has not been integrated into molecular understanding. We therefore established an experimental animal model for colitic cancer, and used proteomic analysis, based on 2-DE and MALDI-TOF MS, to identify proteins involved in colitic cancer. In our model, 6-week-old C57BL/6J mice were exposed to 15 cycles of dextran sodium sulfate (DSS), with each cycle consisting of 0.7% DSS for 1 week followed by distilled water for 10 days. Colorectal tumors developed in 22 of 24 mice (91.6%), with a tumor multiplicity of 1.727 per tumor-bearing mouse. Comparative 2-DE analysis showed that 38 protein spots were differentially expressed in colon tumors and normal colon. We identified 27 of these proteins, including GRP94, HSC70, enolase, prohibitin, and transgelin. The reduction of transgelin expression in mouse colon tumors was confirmed by Western blotting and immunohistochemistry. We also found that transgelin expression was significantly reduced in human colon tumors compared with adjacent non-tumorous tissues. In conclusion, these results suggest that loss of transgelin could be a candidate for biomarker of repeated colitis-associated colon cancer.

Original languageEnglish
Pages (from-to)1158-1165
Number of pages8
Issue number4
Publication statusPublished - 2006 Feb

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology


Dive into the research topics of 'Loss of transgelin in repeated bouts of ulcerative colitis-induced colon carcinogenesis'. Together they form a unique fingerprint.

Cite this