MicroRNA-155 regulates cervical cancer via inducing Th17/Treg imbalance

被引:2
|
作者
Zhang, Y. [1 ]
Wang, Z. -C. [1 ]
Zhang, Z. -S. [1 ]
Chen, F. [1 ]
机构
[1] Peoples Hosp Weifang, Dept Gynecol, Weifang, Peoples R China
关键词
Cervical cancer; MicroRNA-155; Immune regulation; Th17/Treg; T-CELLS; TH17; CELLS; EXPRESSION PROFILES; BREAST-CANCER; DIFFERENTIATION; MIGRATION; CYTOKINE; SOCS1; PREVALENCE; GENERATION;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
OBJECTIVE: To explore the effect of microRNA-155 on cervical cancer and its underlying mechanism. PATIENTS AND METHODS: Peripheral blood and cervical cancer tissues were collected. We used quantitative Real-time polymerase chain reaction (qRT-PCR) to detect expressions of microRNA-155, SOCS1, Th17-related genes (ROR gamma t, IL-17A, IL-21, and IL-22), and Treg-related genes (foxp3, TGF-beta, IL-10, and IL-35) in peripheral blood and cervical cancer tissues. Western blot was used to detect protein expressions of ROR gamma t and foxp3. The proportions of Th17 and Treg cells in CD4+ T cells were measured by flow cytometry. Moreover, IL-17 expression was detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: MicroRNA-155 was overexpressed in peripheral blood and cervical cancer tissues of patients with cervical cancer compared with those of normal controls. Th17-related transcription factors and cytokines in cervical cancer tissues were remarkably elevated than those of normal controls, including ROR gamma t, IL-17, and IL-6. Treg-related transcription factors and cytokines obtained the similar results. Besides, the proportion of Th17 cells in CD4+ T cells was higher in cervical tissues than that of normal controls. In vitro experiments suggested that overexpressed microRNA-155 can inhibit the expression of target gene SOCS1, promote the differentiation of Th17 and increase levels of IL-17, ROR gamma t, and STAT3. CONCLUSIONS: MicroRNA-155 is involved in the occurrence and progression of cervical cancer via inhibiting SOSC1 expression and inducing Th17/Treg imbalance.
引用
收藏
页码:3719 / 3726
页数:8
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