CKAP2 promotes cervical cancer progression by modulating the tumor microenvironment via NF-κB signaling

Luopei Guo; Chunbo Li; Jingjing Guo; Junjun Qiu; Keqin Hua

CKAP2 promotes cervical cancer progression by modulating the tumor microenvironment via NF-κB signaling

Am J Cancer Res. 2023 Jun 15;13(6):2376-2391. eCollection 2023.

Authors

Luopei Guo¹, Chunbo Li¹, Jingjing Guo¹, Junjun Qiu¹, Keqin Hua^{1

2}

Affiliations

¹ Obstetrics and Gynecology Hospital of Fudan University Shanghai, China.
² Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases Shanghai, China.

PMID: 37424820
PMCID: PMC10326565

Abstract

This study aimed to investigate whether CKAP2 could promote cervical cancer (CC) progression by modulating the tumor microenvironment (TME) via NF-κB signaling. The communication between cervical cancer cells and the TME, including THP-1 and HUVECs, was tested. Gain- and loss-of-function assays were performed to elucidate the role of CKAP2 in cervical cancer progression. Western blot analysis was exploited to investigate the potential involved mechanism involved. Here, we reported that cervical cancer tissues were enriched with macrophages and microvessels. CKAP2 increased the tumor-promoting macrophage population. The overexpression of CKAP2 not only promoted endothelial cell viability and tube formation but also increased vascular permeability, and vice versa. Moreover, CKAP2 promoted cervical cancer progression via NF-κB signaling. This effect could be blocked by the NF-κB signaling inhibitor JSH-23. Our findings indicated that CKAP2 could promote cervical cancer progression by modulating the TME via NF-κB signaling.

Keywords: CKAP2; HUVEC; TAM; Tumor microenvironment; angiogenesis; metastasis.