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Volume10, Issue 12 (Suppl) J Proteomics Bioinform, an open access journal
ISSN: 0974-276X
Page 27
conferenceseries.com
World Biomarkers & Pharma Biotech 2017
December 07-09, 2017
December 07-09, 2017 | Madrid, Spain
&
20th International Conference on
PHARMACEUTICAL BIOTECHNOLOGY
9th WORLD BIOMARKERS CONGRESS
JOINT EVENT ON
Genetic and epigenetic alterations in chronic colitis malignant transformation
Wancai Yang1,2 and Yonghua Bao1
1University of Illinois at Chicago, USA
2Jining Medical University, China
C hronic colitis malignant transformation is one of major causes to colorectal cancer, but the mechanisms of colitis develops
and how the chronic colitis progress tomalignance is largely unknown. Using a uniquemousemodel, we have demonstrated
that the mice with targeted disruption of the intestinal mucin gene Muc2 spontaneously develop chronic inflammation at
colon and rectum at early age, whose histopathology was similar to ulcerative colitis in human. In the aged mice, Muc2-/-
mice develop colonic and rectal adenocarcinoma accompanying severe inflammation. To determine the mechanisms of the
malignant transformation, we conducted miRNA array on the colonic epithelial cells from Muc2-/- and +/+ mice. MicroRNA
profiling showed differential expression of miRNAs (i.e. lower or higher expression enrichments) in Muc2-/- mice. Based
on relevance to cytokines and cancer, the miRNAs were validate and were found significantly downregulated or upregulated
in human colitis and colorectal cancer tissues, respectively. The targets of the miRNAs were further characterized and their
functions were investigated. More studies from the Muc2-/- mice showed disorder of gut microbiota. Moreover, a novel tumor
suppressor PRSS8 also plays a critical role in colorectal carcinogenesis and progression, for instance, tissue-specific deletion of
the PRSS8 gene resulted in intestinal inflammation and tumor formation in mice. Gene set enrichment analysis showed that
the colitis and tumorigenesis were linked to the activation of Wnt/beta-catenin, PI3K/AKT and EMT (epithelial-mesenchymal
transition) signaling pathways. Taken above, the disorder of gut microbiota could result in genetic mutations, epigenetic
alterations, leading to the activation of oncogenic signaling, in colorectal epithelial cells, and finally, to colitis development,
promoting malignant transformation and mediating colorectal cancer metastasis.
Biography
Wancai Yang is the Dean of the Institute of Precision Medicine and School of Basic Medical Sciences, Jining Medical University, China, and a Professor of
Pathology, University of Illinois at Chicago, USA. He is also an Adjunct Professor of Biological Sciences, University of Texas, El Paso, USA. He obtained his MD
degree and was trained as a Pathologist from China and received Post-doctoral training on Cancer Biology from Rockefeller University and Albert Einstein Cancer
Center, US, and was promoted as Assistant Professor. In 2006, he moved to the Department of Pathology, UIC and serving as a Grant Reviewer for the National
Institutes of Health (USA) and the National Nature Science Foundation of China. His research focuses on: (1) the determination of mechanisms of gastrointestinal
carcinogenesis, (2) identification of biomarkers for cancer detection and patient selection for chemotherapy, (3) implication of precision medicine in cancers. He has
published more than 80 peer-reviewed articles and has brought important impact in clinical significance.
Wancai Yang et al., J Proteomics Bioinform 2017, 10:12(Suppl)
DOI: 10.4172/0974-276X-C1-109