title: Interleukin-22 promotes lung cancer cell proliferation and migration via the IL-22R1/STAT3 and IL-22R1/AKT signaling pathways.
abstract: Lung cancer continues to be an enormous burden on current health care systems throughout the world, with more than a million deaths every year. Previous studies have shown that interleukin-22 (IL-22) promotes survival and resistance to chemotherapy in human lung cancer cells. However, the association of IL-22 expression with recurrence of lung cancer is still unclear. In this study, we found that expression of IL-22 was upregulated in tumor tissues and serum from patients with recurrent non-small cell lung cancer (NSCLC) as compared to primary NSCLC samples. Treatment with IL-22 promoted cell proliferation and enhanced migration and invasion in A549 and H125 cell lines. Furthermore, we revealed that phosphorylation of STAT3 and AKT was highly induced by treatment with IL-22 via IL-22R1. IL-22R1 was also consistently overexpressed in recurrent NSCLC tissues. Finally, we found that siRNA-mediated depletion of IL-22R1 completely abrogated the effects of IL-22 treatment on cell proliferation and migration activity in NSCLC cell lines. Our findings indicate that IL-22 and IL-22R1 may be novel therapeutic targets for treatment of advanced NSCLC.
authors.affiliation: Department of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, People's Republic of China.|Electric Power Hospital of Heilongjiang Province, 59 Jianbei Road, Harbin, 150030, People's Republic of China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Bi
authors.affiliation: Department of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, People's Republic of China.
authors.forename: Jingyan
authors.initials: J
authors.lastname: Cao
authors.affiliation: Department of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, People's Republic of China.
authors.forename: Shi
authors.initials: S
authors.lastname: Jin
authors.affiliation: Department of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, People's Republic of China.
authors.forename: Liyan
authors.initials: L
authors.lastname: Lv
authors.affiliation: Department of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, People's Republic of China.
authors.forename: Li
authors.initials: L
authors.lastname: Qi
authors.affiliation: Department of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, People's Republic of China.
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
authors.affiliation: Department of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, People's Republic of China.
authors.forename: Jianxiong
authors.initials: J
authors.lastname: Geng
authors.affiliation: Department of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150081, People's Republic of China. yuyan@ems.hrbmu.edu.cn.
authors.forename: Yan
authors.initials: Y
authors.lastname: Yu
mesh_terms: D002289:Carcinoma, Non-Small-Cell Lung / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000502:physiology*; D006801:Humans; D007378:Interleukins / Q000502:physiology*; D008175:Lung Neoplasms / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D018123:Receptors, Interleukin / Q000378:metabolism*; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D015398:Signal Transduction; D000097043:Interleukin-22
chemical_list: D007378:Interleukins; D051057:Proto-Oncogene Proteins c-akt; D018123:Receptors, Interleukin; D050796:STAT3 Transcription Factor; D000097043:Interleukin-22; C494086:STAT3 protein, human; C415369:interleukin-22 receptor
keywords: AKT; IL-22; Metastasis; Non-small cell lung cancer (NSCLC); Recurrence; STAT3