Analysis of LINC01314 and miR-96 Expression in Colorectal Cancer Patients via Tissue Microarray-Based Fluorescence In Situ Hybridization

Author:

Zhang Runan1ORCID,Zhang Genhua2,Li Baohua1,Wang Juan1,Wang Jvfang1,Che Jia1,Wang Xiaojun1,Zhang Zhen1ORCID

Affiliation:

1. Department of Clinical Laboratory, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang, China

2. Department of Pathology, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang, China

Abstract

Background and Objective. Long noncoding RNAs (lncRNAs) have attracted increasing attention as novel biomarkers facilitating early diagnosis, prognostic predictions, and treatment of colorectal cancer (CRC). LINC01314 is aberrantly expressed in many cancers, suggesting its role in tumor development. However, its expression and underlying molecular mechanism in CRC remain to be clarified. The aim of this study was to evaluate the expression levels of LINC01314 and its potentially interacting microRNA (miRNA) miR-96 in CRC patients, as well as clinical values. Methods. A tissue microarray (TMA) containing 76 individual colorectal tumor samples and 28 adjacent normal samples was constructed, and the expression levels of LINC01314 and miR-96 were detected by fluorescence in situ hybridization. Results. The expression levels of both LINC01314 and miR-96 were upregulated in CRC tissues and were associated with vascular metastasis ( p < 0.05 ). A significantly positive correlation was observed between LINC01314 and miR-96 expression in tumor tissues ( p < 0.001 , r = 0.870 ). Dominant expression of LINC01314 was a risk factor for both blood vessel invasion ( p < 0.05 ) and poor 5-year survival ( p = 0.001 , hazard ratio = 4.144 ). The Kaplan–Meier analysis indicated that patients with LINC01314-dominant expression exhibited worse 5-year survival rates than those with miR-96-dominant expression ( p < 0.05 ). Conclusion. The expression patterns of both LINC01314 and miR-96 may be diagnostic of, and prognostic for, CRC. These findings will facilitate further exploration of the molecular mechanism of lncRNAs in CRC.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Biochemistry (medical),Clinical Biochemistry,Genetics,Molecular Biology,General Medicine

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