Colony‑stimulating factor 1 receptor inhibition blocks macrophage infiltration and endometrial cancer cell proliferation Corrigendum in /10.3892/mmr.2020.11197

Hua,Fu; Tian,Ye; Gao,Yingchun; Li,Changhua; Liu,Xiaoping

doi:10.3892/mmr.2019.9963

Colony‑stimulating factor 1 receptor inhibition blocks macrophage infiltration and endometrial cancer cell proliferation

Corrigendum in: /10.3892/mmr.2020.11197

Authors:
- Fu Hua
- Ye Tian
- Yingchun Gao
- Changhua Li
- Xiaoping Liu
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Affiliations: Department of Radiotherapy and Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China, Department of Gynecology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China
Published online on: February 18, 2019 https://doi.org/10.3892/mmr.2019.9963
Pages: 3139-3147
Copyright: © Hua et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Tumor‑associated macrophages (TAMs) promote the progression of endometrial cancer (EC), but the mechanism of TAM in EC cell proliferation remains unclear. It was found that colony stimulating factor (CSF)‑1 and CSF‑1 receptor (CSF‑1R) were highly expressed in EC tissues of patients and two EC cell lines (ECC‑1 and HEC‑1A). Using wound‑healing and chemotactic migration assays to evaluate the role of EC cells in the induction of macrophage migration, it was found that the supernatant of EC cells promoted macrophage cell line (U937) migration; however, the migration capacity of U937 weakened when CSF‑1R was blocked. Subsequently, inhibition of CSF‑1 expression in EC cells also restrained U937 migration. Additionally, blocking CSF‑1R by PLX3397 treatment in U937 cells inhibited EC cell proliferation in a co‑culture system by inhibiting the expression of proliferation‑associated proteins (Janus kinase‑1, phosphoinositide 3‑kinase, AKT, cyclin kinase 2, 4 and retinoblastoma‑associated protein). Together, these results demonstrated that CSF‑1 secreted by EC cells promoted macrophage migration; similarly, CSF‑1‑stimulated macrophages promoted EC cell proliferation. These results suggested that the interaction between CSF‑1 and its receptor served an important role in promoting macrophage infiltration and progression of EC.

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