EphA2 Promotes the Development of Cervical Cancer through the CXCL11/PD-L1 Pathway

Author:

Zhao Xinyue123ORCID,Liu Jiaxi1ORCID,Jin Dongdong1ORCID,Ren Chenchen123ORCID,Yang Li1ORCID,Zhu Yuanhang123ORCID,Huang Changhao4ORCID,Ding Leilei1ORCID,Wu Zimeng1ORCID,Shen Ke1ORCID,Zhang Zhen’an1ORCID,Chen Huanhuan1ORCID,Wang Nannan1ORCID

Affiliation:

1. Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, China

2. Zhengzhou Key Laboratory of Cervical Disease, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, China

3. National Clinical Research Center for Obstetrics and Gynecology, Henan Branch, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, China

4. Organ Transplant Center, Xiangya Hospital, Central South University, Changsha, China

Abstract

Erythropoietin-producing hepatoma receptor A2 (EphA2), receptor tyrosine kinase, the most widespread member of the largest receptor tyrosine kinase family, plays a critical role in physiological and pathological conditions. In recent years, the role of EphA2 in the occurrence and development of cancer has become a research hotspot and is considered a promising potential target. Our previous studies have shown that EphA2 has an indisputable cancer-promoting role in cervical cancer, but its related mechanism requires further research. In this study, high-throughput sequencing was performed on EphA2 knockdown cervical cancer cells and the control group. An analysis of differentially expressed genes revealed that EphA2 may exert its cancer-promoting effect through C-X-C motif chemokine ligand 11 (CXCL11). In addition, we found that EphA2 could further regulate programmed cell death ligand 1 (PD-L1) through CXCL11. This has also been further demonstrated in in vivo experiments. Our study demonstrated that EphA2 plays a tumor-promoting role in cervical carcinoma through the CXCL11/PD-L1 pathway, providing new guidance for the targeted therapy and combination therapy of cervical carcinoma.

Publisher

Hindawi Limited

Subject

Oncology

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