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Knockdown of EPHA1 using CRISPR/CAS9 suppresses aggressive properties of ovarian cancer cells

Cui, Yuxin, Wu, B, Flamini, V ORCID:, Evans, Bronwen A.J. ORCID:, Zhou, D and Jiang, Wen Guo ORCID: 2017. Knockdown of EPHA1 using CRISPR/CAS9 suppresses aggressive properties of ovarian cancer cells. Anticancer Research 37 (8) , pp. 4415-4424. 10.21873/anticanres.11836

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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.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: R Medicine > R Medicine (General)
Publisher: International Institute of Anticancer Research (IIAR)
ISSN: 0250-7005
Funders: Cancer Research Wales
Date of First Compliant Deposit: 15 January 2018
Date of Acceptance: 9 June 2017
Last Modified: 08 May 2023 22:20

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