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全基因组RNA测序数据集揭示了SEVER作为一种新的预后长链非编码RNA及其在结肠腺癌患者中的潜在分子机制。

Genome-wide RNA-sequencing dataset reveals sever as a novel prognostic long non-coding RNA and its potential molecular mechanisms in patients with colon adenocarcinoma.

作者信息

Liao Cun, Gu Zhiwen, Huang Wei, Gong Yizhen, Liao Xiwen, Lin Minglin, Zhang Sen

机构信息

Department of Colorectal and Anal Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi Zhuang Autonomous Region, People's Republic of China.

Guangxi Key Laboratory of Enhanced Recovery after Surgery for Gastrointestinal Cancer, Nanning, 530021, Guangxi Zhuang Autonomous Region, People's Republic of China.

出版信息

J Cancer. 2023 Jul 31;14(12):2386-2398. doi: 10.7150/jca.83424. eCollection 2023.

Abstract

: Through data analysis, we observed that is markedly imbalance between colon adenocarcinoma (COAD) cancer and paracancerous tissues. However, the prognostic value and potential molecular mechanism of in COAD are still unclear. Whole genome RNA-sequencing datasets of The Cancer Genome Atlas (TCGA) COAD cohort were collected into current study, comprehensive survival analysis and bioinformatics function enrichment analysis approaches were apply to explore the clinical outcome and molecular mechanisms of in COAD. In current study, we found that AC096751.1 is markedly down-regulated in COAD cancer tissues (log2 fold change =2.303, <0.0001, false discovery rate <0.0001), and can be serve as a biomarker to distinguish COAD cancer and paracancerous tissues [area under curve=0.9518, 95% confidence interval (CI)=0.9261-0.9776]. Survival analysis suggests that low expression of AC096751.1 is connected with poor clinical outcome of COAD, and can serve as a novel prognostic indicator (log-rank P=0.016, adjusted P=0.005, hazard ratio=0.548, 95% CI=0.360-0.836). Bioinformatics function enrichment analysis suggests that the molecular mechanism of AC096751.1 in COAD may include participation in cell adhesion, cell proliferation, mitogen-activated protein kinase kinase (MAPKK), MAPK, janus-activated kinase-singal transducers and activators of transcriprion cascade, Erk1 and Erk 2 cascade, and nuclear factor-kappa B pathway. Tumor microenvironment and immune infiltration analysis indicates that COAD patients with different AC096751.1 expression have significant variation in tumor immune background. The present study found that is significantly differentially expressed in COAD and can be serve as a novel prognostic biomarker.

摘要

通过数据分析,我们观察到结肠癌(COAD)癌组织与癌旁组织之间存在明显失衡。然而,其在COAD中的预后价值和潜在分子机制仍不清楚。本研究收集了癌症基因组图谱(TCGA)COAD队列的全基因组RNA测序数据集,应用综合生存分析和生物信息学功能富集分析方法来探索其在COAD中的临床结局和分子机制。在本研究中,我们发现AC096751.1在COAD癌组织中显著下调(log2倍数变化=2.303,<0.0001,错误发现率<0.0001),并且可作为区分COAD癌组织和癌旁组织的生物标志物[曲线下面积=0.9518,95%置信区间(CI)=0.9261-0.9776]。生存分析表明,AC096751.1低表达与COAD的不良临床结局相关,并且可作为一种新的预后指标(对数秩检验P=0.016,校正P=0.005,风险比=0.548,95%CI=0.360-0.836)。生物信息学功能富集分析表明,AC096751.1在COAD中的分子机制可能包括参与细胞黏附、细胞增殖、丝裂原活化蛋白激酶激酶(MAPKK)、MAPK、janus活化激酶-信号转导和转录激活因子级联反应、Erk1和Erk2级联反应以及核因子-κB途径。肿瘤微环境和免疫浸润分析表明,不同AC096751.1表达的COAD患者在肿瘤免疫背景方面存在显著差异。本研究发现其在COAD中显著差异表达,并且可作为一种新的预后生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a25/10414039/f963d62afd0c/jcav14p2386g001.jpg

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