Potential Role of LINC00996 in Colorectal Cancer: a Study Based on Data Mining and Bioinformatics

Overview

Journal Onco Targets Ther

Publisher Dove Medical Press

Specialty Oncology

Date 2018 Aug 28

PMID 30147336

Citations 30

Authors

Hua Ge

Yan Yan

Di Wu

Yongsheng Huang

Fei Tian

Affiliations

Soon will be listed here.

Abstract

Background: The clinical significance of LINC00996 in colorectal cancer (CRC) has not been verified. In the current study, the authors aimed to explore the expression of LINC00996 and its clinical significance in CRC based on the data mining of Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) datasets, as well as to elucidate the functions of its potential target genes.

Materials And Methods: GEO and TCGA microarray datasets were used to evaluate the LINC00996 expression and its clinical significance in CRC. LINC00996 related genes were identified by Multi Experiment Matrix, RNA-Binding Protein DataBase, and The Atlas of Noncoding RNAs in Cancer. Subsequently, they were sent to gene ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analysis.

Results: LINC00996 is significantly decreased in CRC tissues compared with non-tumor tissues. Low level of LINC00996 is associated with remote metastasis and poor overall survival. However, LINC00996 has a minimal effect on gender, lymphatic invasion, tumor size, lymph node metastasis, and pathological stage. One hundred and forty-two LINC00996 related genes were identified; the results of functional analysis indicated that LINC00996 might repress tumorigenesis and metastasis via modulating the JAK-STAT, NF-κB, HIF-1, TLR, and PI3K-AKT signaling pathways.

Conclusion: Our study demonstrates that decreased LINC00996 expression may be involved in colorectal carcinogenesis and metastasis, and the depletion of LINC00996 is associated with a poor outcome in CRC patients. Moreover, the JAK-STAT, NF-κB, HIF-1, TLR, and PI3K-AKT pathways may be the key pathways regulated by LINC00996 in CRC.

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