Knockdown of EPHA1 Using CRISPR/CAS9 Suppresses Aggressive Properties of Ovarian Cancer Cells
| Autor: | Wen Guo Jiang, Yuxin Cui, Flamini, B O Wu, Deshan Zhou, Bronwen Alice James Evans |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cancer Research Gene knockdown MMP2 Kinase Erythropoietin-producing hepatocellular (Eph) receptor General Medicine Biology medicine.disease R1 03 medical and health sciences 030104 developmental biology Oncology Cell culture Immunology Extracellular Cancer research medicine Signal transduction Ovarian cancer |
| Zdroj: | Anticancer Research. 37 |
| ISSN: | 1791-7530 0250-7005 |
| DOI: | 10.21873/anticanres.11836 |
| Popis: | Background/Aim: Overexpression of erythropoietin-producing hepatocellular A1 (EPHA1), a member of the EPH super family, is frequently observed in various cancer types. The dysregulated interaction of EPHA1 with its ligand Ephrin A1 has been linked to the progression of ovarian cancer (OC). However, the contribution of EPHA1 in the regulation of the aggressive properties of OC cells remains unknown. Materials and Methods: In this study we investigated the differential expression of EPHA1 in human OC cells. The EPHA1 gene was knocked-down using the CRISPR/Cas9 technique to evaluate its effect on the progressive properties of OC cells. Results: After EPHA1 was knocked-down using a CRISPR/CAS9 genomic editing system in OC cells (SKOV3 and COV504), we observed cell-cycle arrest at the G0/G1 phases in both OC cell lines. Knockdown of EPHA1 in the two OC cells inhibited their aggressive traits, including proliferation, invasion and migration, as well as improving their attachment to extracellular matrix. EPHA1 may play a role in OC through its regulation of multiple signaling pathways, such as matrix metalloproteinase-2 (MMP2), extracellular signal-regulated kinase 2 (ERK2) and proto-oncogene c-MYC. Conclusion: EPHA1 may promote the aggression of some OC cells and, thus, be considered a potential therapeutic target for the treatment of malignant OC. |
| Databáze: | OpenAIRE |
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