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B cell transposition gene 3 (BTG3) is reported to be a tumor suppressor and suppresses proliferation and cell cycle progression. This study aims to analyze the clinicopathological and prognostic significances, and signal pathways of BTG3 mRNA expression in human beings through bioinformatics analysis. We analyzed BTG3 expression using Oncomine, TCGA (the cancer genome atlas), Xiantao, UALCAN (The University of ALabama at Birmingham Cancer data analysis Portal) and Kaplan-Meier plotter databases. Down-regulated BTG3 expression was observed in lung and breast cancers, compared with normal tissues (p < 0.05), but not for gastric and ovarian cancer (p < 0.05). The methylation of BTG3 was shown to be adversely correlated with its mRNA expression (p < 0.05). BTG3 expression was higher in gastric intestinal-type than diffuse-type carcinomas, G1 than G3 carcinomas (p < 0.05), in female than male cancer patients, T1-2 than T3-4, and adenocarcinoma than squamous cell carcinoma of lung cancer (p < 0.05), in invasive ductal than lobular carcinoma, N0 than N1 and N3, TNBC (triple-negative breast cancer) than luminal and Her2+, and Her2+ than luminal cancer of breast cancer (p < 0.05), and G3 than G2 ovarian carcinoma (p < 0.05). BTG3 expression was positively related to the survival rate of gastric and ovarian cancer patients (p < 0.05), but not for breast cancer (p < 0.05). KEGG and PPI (protein-protein interaction) analysis showed that the BTG3 was involved in cell cycle and DNA replication, digestion and absorption of fat and protein, spliceosome and ribosome in cancer. BTG3 expression was positively linked to carcinogenesis, histogenesis, and aggressive behaviors, and was employed to evaluate the prognosis of cancers by regulating cell cycle, metabolism, splicing and translation of RNA. [ABSTRACT FROM AUTHOR]

B cell transposition gene 3 (BTG3) is reported to be a tumor suppressor and suppresses proliferation and cell cycle progression. This study aims to analyze the clinicopathological and prognostic significances, and signal pathways of BTG3 mRNA expression in human beings through bioinformatics analysis. We analyzed BTG3 expression using Oncomine, TCGA (the cancer genome atlas), Xiantao, UALCAN (The University of ALabama at Birmingham Cancer data analysis Portal) and Kaplan-Meier plotter databases. Down-regulated BTG3 expression was observed in lung and breast cancers, compared with normal tissues ( p < 0.05), but not for gastric and ovarian cancer ( p < 0.05). The methylation of BTG3 was shown to be adversely correlated with its mRNA expression ( p < 0.05). BTG3 expression was higher in gastric intestinal-type than diffuse-type carcinomas, G 1 than G 3 carcinomas ( p < 0.05), in female than male cancer patients, T 1-2 than T 3-4 , and adenocarcinoma than squamous cell carcinoma of lung cancer ( p < 0.05), in invasive ductal than lobular carcinoma, N 0 than N 1 and N 3 , TNBC (triple-negative breast cancer) than luminal and Her2+, and Her2+ than luminal cancer of breast cancer ( p < 0.05), and G 3 than G 2 ovarian carcinoma ( p < 0.05). BTG3 expression was positively related to the survival rate of gastric and ovarian cancer patients ( p < 0.05), but not for breast cancer ( p < 0.05). KEGG and PPI (protein-protein interaction) analysis showed that the BTG3 was involved in cell cycle and DNA replication, digestion and absorption of fat and protein, spliceosome and ribosome in cancer. BTG3 expression was positively linked to carcinogenesis, histogenesis, and aggressive behaviors, and was employed to evaluate the prognosis of cancers by regulating cell cycle, metabolism, splicing and translation of RNA., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Zheng, Xue, Zhang, Shi and Zhang.)