Interleukin-22 promotes triple negative breast cancer cells migration and paclitaxel resistance through JAK-STAT3/MAPKs/AKT signaling pathways

Shuqian Wang; Yinan Yao; Minya Yao; Peifen Fu; Weilin Wang

doi:10.1016/j.bbrc.2018.07.088

Interleukin-22 promotes triple negative breast cancer cells migration and paclitaxel resistance through JAK-STAT3/MAPKs/AKT signaling pathways

Biochem Biophys Res Commun. 2018 Sep 10;503(3):1605-1609. doi: 10.1016/j.bbrc.2018.07.088. Epub 2018 Jul 23.

Authors

Shuqian Wang¹, Yinan Yao², Minya Yao³, Peifen Fu⁴, Weilin Wang⁵

Affiliations

¹ 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. Electronic address: frog8433@163.com.
² Department of Respiratory Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310003, China. Electronic address: yaoyinanwangyujia@163.com.
³ 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. Electronic address: yminya@163.com.
⁴ Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University, School of Medicine, Hangzhou, Zhejiang, 310003, China. Electronic address: fupeifen@hotmail.com.
⁵ Key Laboratory of Precision Diagnosis and Treatment for Hepatobiliary and Pancreatic Tumor of Zhejiang Province, Division of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, 310003, China. Electronic address: wam@zju.edu.cn.

PMID: 30072097
DOI: 10.1016/j.bbrc.2018.07.088

Abstract

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.

Keywords: Interleukin-22 (IL-22); Target therapy; Triple negative breast cancer (TNBC).

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Antineoplastic Agents, Phytogenic / pharmacology*
Cell Line, Tumor
Cell Movement / drug effects
Drug Resistance, Neoplasm / drug effects*
Female
Humans
Interleukin-22
Interleukins / metabolism*
Janus Kinases / metabolism
MAP Kinase Signaling System / drug effects
Mitogen-Activated Protein Kinases / metabolism
Paclitaxel / pharmacology*
Proto-Oncogene Proteins c-akt / metabolism
STAT3 Transcription Factor / metabolism
Signal Transduction / drug effects*
Triple Negative Breast Neoplasms / drug therapy*
Triple Negative Breast Neoplasms / metabolism
Triple Negative Breast Neoplasms / pathology*

Substances

Antineoplastic Agents, Phytogenic
Interleukins
STAT3 Transcription Factor
STAT3 protein, human
Janus Kinases
Proto-Oncogene Proteins c-akt
Mitogen-Activated Protein Kinases
Paclitaxel