The clinicopathological significances and related signal pathways of BTG3 mRNA expression in cancers: A bioinformatics analysis

Author:

Zheng Hua-Chuan,Xue Hang,Zhang Cong-Yu,Shi Kai-Hang,Zhang Rui

Abstract

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.

Publisher

Frontiers Media SA

Subject

Genetics (clinical),Genetics,Molecular Medicine

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3