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Esophageal cancer is currently one of the most fatal cancers. However, there is no effective treatment. Increasing evidence suggests that interleukin (IL)‐33 has a significant role in tumor progression and metastasis. Currently, the underlying cellular and molecular mechanism of IL‐33 in promoting esophageal squamous cell carcinoma (ESCC) remains unclear. In this study, we investigated whether IL‐33 could induce the epithelial‐mesenchymal transition (EMT) in ESCC. Interleukin‐33 expression was examined in ESCC and corresponding adjacent normal tissues by immunohistochemistry and quantitative real‐time PCR experiments. Elevated IL‐33 levels were observed in ESCC tissues. Further in vitro experiments were undertaken to elucidate the effect of IL‐33 on migration and invasion in KYSE‐450 and Eca‐109 esophageal cancer cells. Knockdown of IL‐33 decreased the metastasis and invasion capacity in esophageal cancer cells, whereas IL‐33 overexpression showed the opposite effect. We then screened CCL2 which is a downstream molecule of IL‐33, and proved that IL‐33 could promote tumor development and metastasis by recruiting regulatory T cells (Tregs) through CCL2, and IL‐33 regulated the expression of CCL2 through transforming growth factor‐β in Treg cells. Knockdown of IL‐33 decreased the development of human ESCC xenografts in BALB/c nude mice. Collectively, we found that the IL‐33/nuclear factor‐κB/CCL2 pathway played an essential role in human ESCC progress. Hence, IL‐33 should be considered as an effective therapy target for ESCC. [ABSTRACT FROM AUTHOR]

Lung adenocarcinoma (LUAD), the most common non‐small‐cell lung cancer, is characterized by a dense lymphocytic infiltrate, which indicates that the immune system plays an active role in the development and growth of this cancer. However, no investigations to date have proposed robust models for predicting survival outcome for patients with LUAD in terms of tumour immunology. A total of 761 LUAD patients were included in this study, in which the database of The Cancer Genome Atlas (TCGA) was utilized for discovery, and the Gene Expression Omnibus (GEO) database was utilized for validation. Bioinformatics analysis and R language tools were utilized to construct an immune prognostic model and annotate biological functions. Lung adenocarcinoma showed a weakened immune phenotype compared with adjacent normal tissues. Immune‐related gene sets were profiled, an immune prognostic model based on 2 immune genes (ANLN and F2) was developed with the TCGA database to distinguish cases as having a low or high risk of unfavourable prognosis, and the model was verified with the GEO database. The model was prognostically significant in stratified cohorts, including stage I‐II, stage III‐IV and epidermal growth factor receptor (EGFR) mutant subsets, and was considered to be an independent prognostic factor for LUAD. Furthermore, the low‐ and high‐risk groups showed marked differences in tumour‐infiltrating leucocytes, tumour mutation burden, aneuploidy and PD‐L1 expression. In conclusion, an immune prognostic model was proposed for LUAD that is capable of independently identifying patients at high risk for poor survival, suggesting a relationship between local immune status and prognosis. [ABSTRACT FROM AUTHOR]