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Knockdown of EPHA1 by CRISPR/CAS9 Promotes Adhesion and Motility of HRT18 Colorectal Carcinoma Cells
- Source :
- Anticancer research. 36(3)
- Publication Year :
- 2016
-
Abstract
- Erythropoietin-producing hepatocellular A1 (EPHA1) is the first member of the EPH superfamily. Its abnormal expression has been reported in various cancer types. However, the contribution of EPHA1 to the regulation of colorectal cancer cell behaviour remains unknown.In this study, we investigated the expression profile of EPHA1 in human colorectal cancer and its effect on the adhesion and motility of colorectal cancer cells. We used human colorectal cancer specimens and the colorectal adenocarcinoma cell line HRT18 for this purpose.Our cohort screening data showed that in patients with colorectal cancer, low expression of EPHA1 gene is correlated with a remarkably reduced survival. After EPHA1 is knocked-down in colorectal cancer cells using a clustered regularly interspaced short palindromic repeats-associated nuclease 9 (CRISPR-CAS9) genomic editing system, we observed an increase in the spreading and adhesion of HRT18 cells. Moreover, protein array data indicated that the extracellular-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) signaling pathways were activated as a consequence. Inhibition of ERK and JNK proteins with specific inhibitors led to suppression of migration of the colorectal cancer cells.EPHA1 suppresses spreading and adhesion of HRT18 colorectal cancer cells through deactivation of ERK and JNK signaling pathways.
- Subjects :
- Time Factors
Receptor, EphA1
JNK Mitogen-Activated Protein Kinases
Kaplan-Meier Estimate
Adenocarcinoma
Transfection
Enzyme Activation
Gene Expression Regulation, Neoplastic
Cell Movement
Cell Line, Tumor
Gene Knockdown Techniques
Cell Adhesion
Humans
Neoplasm Invasiveness
CRISPR-Cas Systems
Colorectal Neoplasms
Extracellular Signal-Regulated MAP Kinases
Cell Shape
Protein Kinase Inhibitors
Signal Transduction
Subjects
Details
- ISSN :
- 17917530
- Volume :
- 36
- Issue :
- 3
- Database :
- OpenAIRE
- Journal :
- Anticancer research
- Accession number :
- edsair.pmid..........4ec9bc7bdf0ce3a6c68d90a7d58da8f4