world-biomarkers-pharma-biotech-2017-tracks

4 / 28

Notes:
Volume10, Issue 12 (Suppl) J Proteomics Bioinform, an open access journal
ISSN: 0974-276X
Page 28
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 deficiency of PRSS8 causes mouse intestinal inflammation and tumors
Yonghua Bao1 and Wancai Yang1,2
1Jining Medical University, China
2University of Illinois at Chicago, USA
PRSS8 is a glycosylphosphatidylinositol anchored serine protease, has physiological and pathophysiological functions
and shows important roles in the epidermal barrier function and in the regulation of glucose homeostasis. However, the
biological functions of PRSS8 in cancer initiation and progression is unknown. We have found that PRSS8 was significantly
reduced in esophageal and colorectal cancers and acted as a tumor suppressor in colitis-associated colorectal cancer through
targeting Sphk1/Stat3/Akt signaling pathway. To determine the roles of PRSS8 in colorectal cancer in vivo, we developed a
conditional knockout mouse model - intestine-specific deletion of Prss8 in mice (Prss8 fl/fl-Cre+, Prss8 CKO), and found that
PRSS8 deletion caused spontaneous formation of intestinal inflammation and tumors. At the age of 3 months, about 20% of
the Prss8 CKO mice exhibited inflamed rectum and then exerted rectal prolapse. Histopathologic analysis showed that 65%
Prss8 CKO mice had developed chronic inflammation in large intestine at 3 months. Interestingly, 45% Prss8 CKO mice had
developed hyperplasia in small intestine at 3 months. At the age of 6 months, 53 % of the Prss8 CKOmice developed adenomas,
and at the age of 9 months, 75% of the Prss8 CKO mice developed adenomas. Further studies showed that gastrointestinal
tumorigenesis was linked to the disruption of intestinal epithelial cell maturation: more proliferative cells and moved faster
in the Prss 8 CKO mouse, assayed by BrdU staining and migration assay. Moreover, Prss 8 CKO mouse intestine exhibited
less mature mucin drops and goblet cells at the crypts of small and large intestine in comparison with the WT mice. Gene
profile using mouse intestinal epithelial cells and gene set enrichment analysis showed that the tumorigenesis was associated
with oncogenic signaling pathways, including Wnt/beta-catenin and inflammatory signaling. The underlying mechanisms are
under further investigation.
Biography
Yonghua Bao graduated from Jiamusi Medical University (China) with a Clinical Medicine background, received PhD on Biochemistry and Molecular Biology from
Jilin University and Post-doctoral training on Biochemistry and Molecular Biology in the State Key Laboratory of China Agricultural University. She was promoted as
Associate Professor and worked in cancer and cell signal transduction lab since 2012. She was recruited by Jining Medical University as a Professor of Pathology
in 2015, and was appointed as Vice Dean of Institute of Precision Medicine. Her study focuses on cancer biology and cell signaling pathways in gastrointestinal
carcinogenesis, progression and metastasis. As PI, she was funded by the National Natural Science Foundation of China. She has published 22 papers and was
awarded 3 patents.
Yonghua Bao et al., J Proteomics Bioinform 2017, 10:12(Suppl)
DOI: 10.4172/0974-276X-C1-109