Carcinogenesis, Teratogenesis & Mutagenesis ›› 2023, Vol. 35 ›› Issue (5): 341-348.doi: 10.3969/j.issn.1004-616x.2023.05.003

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Expression and biological functions of TGFBI in glioma

GUO Wenjing1, DENG Hui2, SONG Ping2, ZHANG Mengxian2   

  1. 1. Department of Oncology, Xiangyang Central Hospital/Affiliated Hospital of Hubei University of Arts and Science, Xiangyang 441000;
    2. Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China
  • Received:2022-10-09 Revised:2023-04-05 Published:2023-10-13

Abstract: OBJECTIVE:To investigate expression and biological function of the transforming growth factor β-induced protein (TGFBI) in glioma. METHODS: The transcriptome data and the corresponding clinical information of tumor samples from glioma patients in the Cancer Genome Atlas (TCGA)、Chinese Glioma Genome Atlas (CGGA) and Rembrandt database were obtained to analyze potential associations between grades,subtypes, overall survival of glioma patients and TGFBI mRNA expression levels. Expression of TGFBI protein in 35 glioblastoma tissues and 5 normal brain tissues was analyzed using immunohistochemical method. Furthermore, the U87 and U373 cell lines were transfected with the constructed lentivirus vector containing shTGFBI target sequence to establish glioblastoma cell lines with low TGFBI expression and then to explore the effect of TGFBI on tumor proliferation、invasion、apoptosis and cell cycle. Finally,Gene set enrichment assay (GSEA) was used to predict the related pathways that TGFBI might participate in the occurrence and development of glioma. RESULTS: Results from TCGA、CGGA and Rembrandt databases showed that TGFBI expressions were positively correlated with the WHO grades (P<0.05). In addition,high expressions of TGFBI were correlated with inferior survival in glioma patients. Expressions of TGFBI in glioma tissues were significantly higher than that in normal brain tissues (P<0.05). The knockdown of TGFBI significantly inhibited proliferation and invasion of cancer cells、promoted cell apoptosis and promoted cell cycle progression from the G1 to the S phases. GSEA showed that high expressions of TGFBI were involved in activation of the TOLL-like receptors,NOD-like receptors and JAK-STAT signaling pathways. CONCLUSION: Overexpressions of TGFBI in gliomas promoted proliferation and invasion of tumor cells,inhibited cell apoptosis and induced cell cycle rearrangement. Thus,TGFBI might play an oncogene role in the occurrence and development of gliomas.

Key words: glioma, TGFBI, database, immunohistochemistry, prognosis judgment

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