title: Overexpression of the transcription factor FOXP3 in lung adenocarcinoma sustains malignant character by promoting G1/S transition gene CCND1.
abstract: The Forkhead box P3 (FOXP3) transcription factor is the key driver of the differentiation and immunosuppressive function of regulatory T cells (Tregs). Additionally, FOXP3 has been reported to be expressed in many solid tumor cell lines and tissues. However, its role in tumorigenesis and tumor progression is conflicting, both tumor suppressive and promoting functions have been described. In this study, we demonstrated that FOXP3 was expressed in both lung adenocarcinoma tissues and the lung adenocarcinoma cell line A549. FOXP3 inhibition decreased cell proliferation, migration, and invasion as well as the secretion of inhibitory cytokines (e.g., transforming growth factor beta 1 (TGF-β1), interleukin 35 (IL-35), and heme oxygenase-1 (HMOX1)), suggesting a positive role for FOXP3 in tumor development. Importantly, we found that FOXP3 could enhance lung adenocarcinoma cell proliferation via upregulating the levels of the cell cycle G1/S checkpoint gene CCND1. These data demonstrated that FOXP3 could be regarded as a novel therapeutic target for inhibiting lung adenocarcinoma progression.
authors.affiliation: Department of Immunology, College of Basic Medical Science, Jilin University, Changchun, 130021, China.
authors.forename: Yinan
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Immunology, College of Basic Medical Science, Jilin University, Changchun, 130021, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Li
authors.affiliation: Department of Immunology, College of Basic Medical Science, Jilin University, Changchun, 130021, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Yang
authors.affiliation: Department of Immunology, College of Basic Medical Science, Jilin University, Changchun, 130021, China.
authors.forename: Haiying
authors.initials: H
authors.lastname: Fu
authors.affiliation: Department of Immunology, College of Basic Medical Science, Jilin University, Changchun, 130021, China.
authors.forename: Yaqing
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Immunology, College of Basic Medical Science, Jilin University, Changchun, 130021, China. liyi@jlu.edu.cn.
authors.forename: Yi
authors.initials: Y
authors.lastname: Li
mesh_terms: D000072283:A549 Cells; D000230:Adenocarcinoma / Q000235:genetics* / Q000473:pathology; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics* / Q000473:pathology; D002455:Cell Division; D019938:Cyclin D1 / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D016207:Cytokines / Q000378:metabolism; D051858:Forkhead Transcription Factors / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D059585:G1 Phase Cell Cycle Checkpoints / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics* / Q000473:pathology; D009361:Neoplasm Invasiveness; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D034622:RNA Interference; D012334:RNA, Neoplasm / Q000096:biosynthesis / Q000235:genetics; D034741:RNA, Small Interfering / Q000235:genetics; D019139:Tumor Escape / Q000235:genetics / Q000502:physiology; D015854:Up-Regulation
chemical_list: C530104:CCND1 protein, human; D016207:Cytokines; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D009363:Neoplasm Proteins; D012334:RNA, Neoplasm; D034741:RNA, Small Interfering; D019938:Cyclin D1
keywords: CCND1; Cell proliferation; FOXP3; Lung adenocarcinoma