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Th22 Cells/IL-22 Serves as a Protumor Regulator to Drive Poor Prognosis through the JAK-STAT3/MAPK/AKT Signaling Pathway in Non-Small-Cell Lung Cancer.

Abstract
The interaction of immune cells and cytokines in the tumor microenvironment affects the development and prognosis of tumors with an unclear potential regulatory mechanism. Recent studies have elucidated the protumor role of Th22 cells and its lineage-specific cytokine IL-22 in different human cancers. The present study is aimed at investigating the biological effect of Th22 cells/IL-22 and its molecular mechanism in the pathogenesis process of non-small-cell lung cancer (NSCLC). It was initially found that Th22 cells were enriched in the peripheral blood of NSCLC patients. The level of Th22 cells in peripheral blood mononuclear cells (PBMCs) was positively correlated with the TNM stage, lymph node metastasis, and clinical tumor biomarkers. Furthermore, IL-22 not only antagonized the apoptosis inducing and cell cycle arresting effect by chemotherapy and molecular targeted drugs on NSCLC cell lines but also promoted tumor cell proliferation and tumor tissue growth. Moreover, IL-22 activated the JAK-STAT3/MAPK/AKT signaling pathway, both in vitro and in vivo. Conclusively, the present results confirm that Th22 cells/IL-22 may serve as a negative immune regulator in lung cancer.
AuthorsYinan Yao, Guangdie Yang, Guohua Lu, Jiani Ye, Luyun Cui, Zhu Zeng, Junjun Chen, Jianying Zhou
JournalJournal of immunology research (J Immunol Res) Vol. 2022 Pg. 8071234 ( 2022) ISSN: 2314-7156 [Electronic] Egypt
PMID35669104 (Publication Type: Journal Article)
CopyrightCopyright © 2022 Yinan Yao et al.
Chemical References
  • Interleukins
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Proto-Oncogene Proteins c-akt
Topics
  • Carcinoma, Non-Small-Cell Lung (pathology)
  • Cell Line, Tumor
  • Cell Proliferation
  • Humans
  • Interleukins
  • Leukocytes, Mononuclear (metabolism)
  • Lung Neoplasms (pathology)
  • Prognosis
  • Proto-Oncogene Proteins c-akt (metabolism)
  • STAT3 Transcription Factor (metabolism)
  • Signal Transduction
  • Tumor Microenvironment
  • Interleukin-22

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