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CircRNA/mRNA expression data for the different phases of colitis-associated colorectal cancer in a mouse model

ABSTRACT: The causal relationships between inflammation and cancer are now widely recognized and discussed. Epidemiological and experimental studies have shown that patients with inflammatory bowel disease (IBD) are major risk factors for developing CRC than the general population. Approximately 18.4% of patients with IBD are reported to develop into colitis associated cancer (CAC) within 30 years after the onset of disease . CAC has become the major cause of death in IBD patients. While these mechanisms by which chronic inflammation promotes colonic carcinogenesis are being investigated, many unanswered questions remain. Circular RNA (CircRNA) is a newly discovered type of non-coding RNAs, which is involved in the colorectal cancer (CRC) development by diverse mechanisms. In our current study, we employed the widely used Dextran Sodium Sulfate (DSS)-induced acute colitis and Azoxymethane (AOM)/DSS-induced CAC models to screen the circRNA and mRNA expression profiles in inflammation and inflammation-associated cancer by the high throughput sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE166708 | GEO | 2024/02/01

REPOSITORIES: GEO

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Project description:MUC1 is a tumor-associated antigen that is aberrantly expressed in cancer and inflammatory bowel disease (IBD). Even though immune cells express low MUC1 levels, their modulations of MUC1 are important in tumor progression. Consistent with previous clinical data that show increased myeloid-derived suppressor cells (MDSCs) in IBD, we now show that down-regulation of MUC1 on hematopoietic cells increases MDSCs in IBD, similar to our data in tumor-bearing mice. We hypothesize that MDSC expansion in IBD is critical for tumor progression. In order to mechanistically confirm the linkage between Muc1 down-regulation and MDSC expansion, we generated chimeric mice that did not express Muc1 in the hematopoietic compartment (KOM-bM-^FM-^RWT). These mice were used in 2 models of colitis and colitis-associated cancer (CAC) and their responses were compared to wildtype chimeras (WTM-bM-^FM-^RWT). KOM-bM-^FM-^RWT mice show increased levels of MDSCs during colitis that was responsible for the larger colon tumors that eventually developed in these mice. Using microarray and qRT-PCR analysis, we observed increased pro-tumorigenic signaling in the colons of KOM-bM-^FM-^RWT mice during colitis as compared to WTM-bM-^FM-^RWT mice. Our RNA (microarray and qRT-PCR analysis) and protein analysis demonstrate increased up-regulation of metalloproteinases, collagenases, defensins, complements, growth factors, cytokines and chemokines in KOM-bM-^FM-^RWT mice as compared to WTM-bM-^FM-^RWT mice. Antibody-mediated depletion of MDSCs in mice during colitis reduced colon tumor formation during CAC. Development of CAC is a serious complication of colitis and our data highlight MDSCs as a targetable link between inflammation and cancer. A total of 12 samples were analysed. RNA was made from the mucosa of the colon of WTM-bM-^FM-^RWT and KOM-bM-^FM-^RWT mice that were either untreated or treated with azoxymethane (AOM) and dextran sodium sulfate (DSS). There are 4 groups, n=3 for each group: untreated WTM-bM-^FM-^RWT mice, untreated KOM-bM-^FM-^RWT mice, AOM+DSS treated WTM-bM-^FM-^RWT mice, AOM+DSS treated KOM-bM-^FM-^RWT mice = 12 samples in total.

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CircRNA/mRNA expression data for the different phases of colitis-associated colorectal cancer in a mouse model

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