期刊
JOURNAL OF CANCER
卷 12, 期 15, 页码 4638-4647出版社
IVYSPRING INT PUBL
DOI: 10.7150/jca.56185
关键词
cervical cancer; radioresistance; IL-11; radiotherapy
类别
资金
- National Natural Science Foundation of China [81802997, 81602391, 81502666]
- Foundation for Free Exploration of Hubei University of Medicine [FDFR201802]
- Natural Science Foundation of Hubei Province of China [2019CFA034, 2017CFB167, 2018CFB405, 2017CFB456]
- Natural Science Foundation of Hubei Provincial Department of Education [Q20202106, D20172102, Q20162109]
- Innovative Research Program for Graduates of Hubei University of Medicine [YC2019025]
- Scientific and Technological Project of Shiyan City of Hubei Province [19Y40, 16Y19, 17Y10, 17Y12]
IL-11 is upregulated in cervical cancer tissues and associated with clinical stages and poor prognosis. Knocking down IL-11 can reduce radioresistance in Hela cells, while exogeneous IL-11 can confer radioresistance in C33A cells, potentially through the activation of the PI3K/Akt signaling pathway. Therefore, IL-11 may be a promising target for radiosensitization in cervical cancer therapy.
Cervical cancer is one of the most common malignant tumors in the female reproductive system. Radioresistance remains a significant factor that limits the efficacy of radiotherapy for cervical cancer. Interleukin-11 (IL-11) has been reported to be upregulated in various types of human cancer and correlate with clinical stage and poor survival. However, the exact effects and mechanisms of IL-11 in the radioresistance of cervical cancer have not yet been defined. In this research, TCGA databases revealed that IL-11 expression was upregulated in cervical cancer tissues and was associated with clinical stages and poor prognosis in cervical cancer patients. We discovered that IL-11 concentration was significantly upregulated in radioresistant cervical cancer cells. Knocking down IL-11 in Hela cells could reduce clonogenic survival rate, decrease cell viability, induce G2/M phase block, and facilitate cell apoptosis. In contrast, Exogeneous IL-11 in C33A cells could upregulate clonogenic survival rate, increase cell viability, curb G2/M phase block, and cell apoptosis. Mechanistic investigations showed that radioresistance conferred by IL-11 was attributed to the activation of the PI3K/Akt signaling pathway. Altogether, our results demonstrate that IL-11 might be involved in radioresistance, and IL-11 may be a potent radiosensitization target for cervical cancer therapy.
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