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首页> 外文期刊>Journal of cellular physiology. >CCL21/CCR7 interaction promotes EMT and enhances the sternness of OSCC via a JAK2/STAT3 signaling pathway
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CCL21/CCR7 interaction promotes EMT and enhances the sternness of OSCC via a JAK2/STAT3 signaling pathway

机译：CCL21 / CCR7交互促进EMT和增强的严厉OSCC通过JAK2 / STAT3信号通路

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摘要

Chemokines and their receptors show a strong relationship with poor clinical outcomes in various cancers. However, their underlying mechanisms remain to be fully elucidated. In our research, we found C-C chemokine receptor 7 (CCR7) and its ligand chemokine ligand 21 (CCL21) were abnormally abundant in oral squamous cell carcinoma (OSCC) tissues, and CCR7 expression was correlated with poor prognosis of OSCC. After exogenous CCL21 stimulation, epithelial-mesenchymal transition (EMT) was promoted in OSCC cells, and cancer stem cell-related markers CD133, CD44, BMI1, ALDH1A1, and OCT4 increased. The migration, invasion, tumorsphere formation, and colony formation abilities of OSCC cells were enhanced, indicating that the sternness of OSCC cells was also improved. The knockdown and overexpression of CCR7 efficiently affected the CCL21-induced EMT and sternness of OSCC cells. When treated with CCL21, the phospho-JAK2 and phospho-STAT3 markedly increased. The inhibitor of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) significantly suppressed CCL21-induced EMT and sternness of OSCC cells. In conclusion, CCL21/CCR7 axis regulated EMT progress and promoted the sternness of OSCC by activating the JAK2/STAT3 signaling pathway. CCL21/CCR7 might be an effective target for OSCC prevention and treatment.
机译：趋化因子及其受体表现出强劲与贫穷的临床结果之间的关系各种癌症。机制仍有待阐明。研究中,我们发现碳碳趋化因子受体7(其)及其配体趋化因子配体21 (CCL21)异常丰富的口腔鳞状细胞癌(OSCC)组织,CCR7表达与OSCC的不良预后相关。外生CCL21刺激,epithelial-mesenchymal过渡(EMT)提升在OSCC细胞,癌症干细胞闲暇的标志物CD133, CD44, BMI1 ALDH1A1,和OCT4增加。tumorsphere形成和集落形成OSCC细胞的能力增强,表明的严厉也是OSCC细胞改善。CCR7有效地影响CCL21-induced EMT和严厉OSCC细胞。CCL21, phospho-JAK2 phospho-STAT3明显增加。激酶2 /信号传感器和催化剂转录显著3 (JAK2 / STAT3)抑制CCL21-induced EMT和严厉的OSCC细胞。监管EMT的进步,促进了严厉OSCC的激活JAK2 / STAT3信号途径。OSCC预防和治疗。

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