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Co-expression of HGFR and CD133 cancer stem cell marker in subepithelial cells of chronically active ulcerative colitis

Date

10 Oct 2016

Session

Poster display

Presenters

Ferenc Sipos

Citation

Annals of Oncology (2016) 27 (6): 1-14. 10.1093/annonc/mdw362

Authors

F. Sipos, Z. Tulassay, G. Műzes

Author affiliations

  • 2nd Department Of Medicine, Semmelweis University, 1088 - Budapest/HU
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Resources

Abstract 958

Background

Chronic, longstandig inflammation is known to be a hallmark of cancer. Colorectal cancer risk is elevated in longstanding ulcerative colitis (UC). Previously, we found that in active, newly diagnosed UC HGFR+ circulating and subepithelial cells display an expression profile characteristics for mesenchymal-epitehlial transition. The aim of this study was to characterize the regeneration-associated stem cell-related phenotype of hepatocyte-derived growth factor receptor (HGFR)-expressing cells in longstanding, chronically active UC.

Methods

Forty matched peripheral blood and colonic biopsy samples from 20 patients with chronically active UC and 20 healthy controls were collected. After preparing tissue microarrays and blood smears HGFR, CDX2, CD133 and Musashi-1 conventional and double fluorescent immunolabelings were performed, then the samples were digitalized. For semiquantitative counting of immunopositive lamina propria (LP) and blood cells were counted, then mean ± SD were determined. Using laser microdissection subepithelial cells from the lamina propria were collected. Gene expression analysis of HGFR, CD133, CDX2, Lgr5, Musashi-1 and CK20 were performed in all samples by using real-time RT-PCR.

Results

Higher number of HGFR (blood: 7.4 ± 1.3 vs 28.4 ± 2.23; LP: 2.4 ± 0.7 vs 8.15 ± 0.59; P 

Conclusions

In chronically active UC, the portion of circulating and subeithelial HGFR-expressing cells decreased, indicating a lower activity of mucosal regeneration by mesenchymal-epithelial transition. However, the higher number of HGFR/CD133 double positive cells may indicate the involvement of CD133 expression in colitis-associated carcinogenesis.

Clinical trial identification

Legal entity responsible for the study

Ferenc Sipos

Funding

Hungarian Scientific Research Fund (OTKA-K111743 grant)

Disclosure

All authors have declared no conflicts of interest.

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