ArticleJournal of cellular and molecular medicine2021
EphA2 promotes tumorigenicity of cervical cancer by up-regulating CDK6.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The trial behind it
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- Synthesis and Biological Evaluation of Isomeric Artemisinin Trimers as Novel Antitumor Agents.Molecules (Basel, Switzerland) · 2026Article
- Unsupervised Machine Learning Reveals Temporal Components of Gene Expression in HeLa Cells Following Release from Cell Cycle Arrest.International journal of molecular sciences · 2025Article
- Review
- DDR1 promotes metastasis of cervical cancer and downstream phosphorylation signal via binding GRB2.Cell death & disease · 2024Article
- Unraveling the role of EPHA2 in regulating migration and immunomodulation processes in cervical cancer: exploring the synergic effect of 17β-estradiol on cancer progression.Medical oncology (Northwood, London, England) · 2024Article
- The EphA2 Receptor Regulates Invasiveness and Drug Sensitivity in Canine and Human Osteosarcoma Cells.Cells · 2024Article
- Puzzling out the role ofNon-coding RNA research · 2024Review
- Targeting EphA2: a promising strategy to overcome chemoresistance and drug resistance in cancer.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Eph receptors and ephrins in cancer progression.Nature reviews. Cancer · 2024Review
- Review
- Remodeling the tumor immune microenvironment via siRNA therapy for precision cancer treatment.Asian journal of pharmaceutical sciences · 2023Review
- The EPH/Ephrin System in Gynecological Cancers: Focusing on the Roots of Carcinogenesis for Better Patient Management.International journal of molecular sciences · 2022Review
- EphA2 Promotes the Development of Cervical Cancer through the CXCL11/PD-L1 Pathway.Journal of oncology · 2022Article
- Fully human recombinant antibodies against EphA2 from a multi-tumor patient immune library suitable for tumor-targeted therapy.Bioengineered · 2021Article
- High-Risk Human Papillomavirus and Epstein-Barr Virus Coinfection: A Potential Role in Head and Neck Carcinogenesis.Biology · 2021Review
- circ-ZNF609: A potent circRNA in human cancers.Journal of cellular and molecular medicine · 2021Review
- EphA2 promotes tumorigenicity of cervical cancer by up-regulating CDK6.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Erythropoietin-producing hepatocellular receptor A2 (EphA2) receptor tyrosine kinase plays an important role in tissue organization and homeostasis in normal organs. EphA2 is overexpressed in a variety of types of solid tumours with oncogenic functions. However, the role of EphA2 in cervical cancer (CC) is still needed to be further explored. Here, we examined the role of EphA2 by establishing a stable EphA2 knock-down CC cell lines or a stable EphA2-overexpressed CC cells lines. Overexpression of EphA2 increased cell proliferation and migration of CC while EphA2 knock-down decreased the CC tumorigenicity. In addition, EphA2 knock-down suppressed CC tumour development in the xenograft mouse model. Inhibition of EphA2 by AWL-II-41-27, EphA2-specific tyrosine kinase inhibitor, or knock-down of EphA2 decreased mRNA and protein expression of cyclin-dependent kinase (CDK) 6 in CC cells, which increased cellular susceptibility to epirubicin (EPI), an anti-cancer chemotherapy drug. A clinicopathological study of EphA2 was conducted on a cohort of 158 human CC patients. EphA2 protein expression was positively correlated with CDK6 protein expression, invasion depth, lymph node metastasis and clinicopathological stage (P < .05). This study demonstrates the oncogenic activity of EphA2 in vitro and in vivo, which provides insights into the relevant mechanisms that might lead to novel treatments for CC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.