白细胞介素-22 通过 JAK-STAT3/MAPKs/AKT 信号通路促进三阴性乳腺癌细胞迁移和紫杉醇耐药性。
Interleukin-22 promotes triple negative breast cancer cells migration and paclitaxel resistance through JAK-STAT3/MAPKs/AKT signaling pathways.
机构信息
Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University, School of Medicine, Hangzhou, Zhejiang, 310003, China; Key Laboratory of Precision Diagnosis and Treatment for Hepatobiliary and Pancreatic Tumor of Zhejiang Province, The First Affiliated Hospital, Zhejiang University, School of Medicine, Hangzhou, Zhejiang, 310003, China.
Department of Respiratory Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310003, China.
出版信息
Biochem Biophys Res Commun. 2018 Sep 10;503(3):1605-1609. doi: 10.1016/j.bbrc.2018.07.088. Epub 2018 Jul 23.
PURPOSE
Owing to the absence of any targeted therapies, triple negative breast cancer (TNBC), which accounts for approximately 15% of all breast cancers, typically have a poorer outcome. In an attempt to find out the TNBCs' microenvironment, we ran into the endogenous expression of a newly discovered cytokine known as Interleukin (IL)-22.
METHODS
Thirty TNBC patients were recruited and the levels of IL-22 producing (Th22) cells in tumor, paratumor and normal breast tissues were measured. Then we studied the role and mechanism of IL-22 in migration and paclitaxel resistance in TNBC cells MDA-MB 468 and MDA-MB 231.
RESULTS
The prevalence of Th22 cells were gradually increased in normal, paratumor and tumor tissues. In vitro, IL-22 promotes TNBC cells migration and induces paclitaxel resistance. Importantly, IL-22 exposure of TNBC cells resulted in JAK-STAT3/MAPKs/AKT signaling pathways activated.
CONCLUSION
IL-22 may play an accelerating role in the development of TNBC and may open a new therapeutic approach for TNBC.
目的
由于缺乏靶向治疗，三阴性乳腺癌（TNBC）约占所有乳腺癌的 15%，通常预后较差。为了研究 TNBC 的微环境，我们发现了一种新发现的细胞因子——白细胞介素（IL）-22 的内源性表达。
方法
招募了 30 名 TNBC 患者，测量肿瘤、肿瘤旁和正常乳腺组织中产生 IL-22 的细胞（Th22 细胞）的水平。然后，我们研究了 IL-22 在 TNBC 细胞 MDA-MB 468 和 MDA-MB 231 中的迁移和紫杉醇耐药中的作用和机制。
结果
Th22 细胞在正常、肿瘤旁和肿瘤组织中的发生率逐渐增加。在体外，IL-22 促进 TNBC 细胞的迁移并诱导紫杉醇耐药。重要的是，IL-22 暴露于 TNBC 细胞导致 JAK-STAT3/MAPKs/AKT 信号通路激活。
结论
IL-22 可能在 TNBC 的发展中起加速作用，并为 TNBC 开辟新的治疗方法。
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