Previous studies have showen that

mindin is important in both innate and adaptive immunity. As an ECM, Mindin affects cell adhesion, migration, proliferation and differentiation in different cell type. However, its role during the colon cancer development remains unknown. Methods: To define the function of mindin in carcinogenesis of colon this website cancer, we established the stable cell pools with mindin knockdown or overexpressed based on mice syngenic colorectal CMT93 and CT26 cancer cell line. A model of subcutaneously transplanted stable cell pools in C57BL/6 mice was used to monitor the tumor growth. Results: Silencing of the mindin in CMT93 and CT26 cells showed enhanced abilities of migration, invasion and proliferation compared to the control cells in vitro. In contrast, mindin overexpression cell pools showed the reduction

of migration, invasion and proliferation. Furthermore, we observed that in vivo tumor growth in C57BL/6 mice, and consistent with in vitro finding that mindin knockdown colorectal cancer cells showed the significant greater tumor growth, and overexpression of mindin in colorectal cancer cells attenuated tumor growth compared with control group. Moreover, the phosphorylation levels of Erk1/2 were upregulated in both of mindin knockdown cells and tumor tissues, and downregulated in the mindin overexpressing cells

and tumor tissues compared to the control groups. Conclusion: Our data revealed the novel tumor suppressive function Ceritinib of mindin during colon cancer development learn more and suggested that mindin might be applied as a novel theraputic target for colorectal cancer. Key Word(s): 1. Mindin; 2. Colon cancer; 3. MAPK/ERK; Presenting Author: BAYASI GULENG Additional Authors: YUN-PENG LIU, JIAN-LIN REN Corresponding Author: BAYASI GULENG Affiliations: Zhongshan Hospital affiliated to Xiamen University Objective: EGFR activation and PKM2 expression are instrumental in tumorigenesis. EGFR activation regulates PKM2 functions in a subcellular compartment-dependent manner and promotes gene transcription and tumor growth. In addition, PKM2 is upregulated in EGFR-induced pathways in glioma malignancies. However, we found that PKM2 could also regulate the activity of the EGF/EGFR signaling pathway in gastric cancer cells. We aimed to define the biological mechanisms for PKM2 in regulating the cell motility and invasion. Methods: We employed stable transfection with short hairpin RNA to stably silence the expression of PKM2 in the BGC823, SGC7901 and AGS gastric cancer cell lines. The effects of PKM2 in vitro were determined by assessing cell migration and invasion. Immunohistochemical analysis was used to explore the relationship among PKM2 and other proteins.