EphB6 overexpression and Apc mutation together promote colorectal cancer.
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| Abstract |
The erythropoietin-producing hepatocyte (Eph) family tyrosine kinases play important roles in tumorigenesis and cancer aggression. In this study, we investigated the role of EphB6 in oncogenic transformation of colorectal epithelial cells in vitro and in vivo. EphB6 is upregulated in human colorectal cancer (CRC) tissues as compared to normal tissues, and its overexpression promotes proliferation, migration and invasion by IMCE colorectal adenoma cells, in which one Apc allele is mutated. EphB6 overexpression together with Apc mutation leads to the development of colorectal tumors in vivo. Expression microarrays using mRNAs and lncRNAs isolated from EphB6-overexpresssing IMCE and control cells revealed a large number of dysregulated genes involved in cancer-related functions and pathways. The present study is the first to demonstrate that EphB6 overexpression together with Apc gene mutations may enhance proliferation, invasion and metastasis by colorectal epithelial cells. Microarray data and pathway analysis of differentially expressed genes provided insight into possible EphB6-regulated mechanisms promoting tumorigenesis and cancer progression. EphB6 overexpression may represent a novel, effective biomarker predictive of cell proliferation, invasion and metastasis patterns in CRC tumors.
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| Authors | Dan Xu, Liang Yuan, Xin Liu, Mingqi Li, Fubin Zhang, Xin Yue Gu, Dongwei Zhang, Youlin Yang, Binbin Cui, Jinxue Tong, Jin Zhou, Zhiwei Yu |
| Journal | Oncotarget (Oncotarget) Vol. 7 Issue 21 Pg. 31111-21 (May 24 2016) ISSN: 1949-2553 [Electronic] United States |
| PMID | 27145271 (Publication Type: Journal Article) |
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