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A meta‑analysis and bioinformatics exploration of the diagnostic value and molecular mechanism of miR‑193a‑5p in lung cancer

  • Authors:
    • Zu‑Cheng Xie
    • Rui‑Xue Tang
    • Xiang Gao
    • Qiong‑Ni Xie
    • Jia‑Ying Lin
    • Gang Chen
    • Zu‑Yun Li

  • View Affiliations

  • Published online on: July 19, 2018     https://doi.org/10.3892/ol.2018.9174
  • Pages: 4114-4128

  • Copyright: © Xie et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Lung cancer is a leading cause of mortality worldwide and despite recent improvements in lung cancer treatments patient mortality remains high. miR‑193a‑5p serves a crucial role in the initiation and development of cancer; it is necessary to understand the underlying molecular mechanisms of miR‑193a‑5p in lung cancer, which may enable the development of improved clinical diagnoses and therapies. The present study investigated the diagnostic value of peripheral blood and tissue miR‑193a‑5p expression using a microarray meta‑analysis. Peripheral blood miR‑193a‑5p was revealed to be upregulated in patients with lung cancer. The pooled area under the curve (AUC) was 0.67, with a sensitivity and specificity of 0.74 and 0.56, respectively. Conversely, the peripheral tissue miR‑193a‑5p expression in patients with lung cancer was significantly downregulated. The pooled AUC was 0.83, and the sensitivity and specificity were 0.65 and 0.89, respectively. Through bioinformatics analysis, three Kyoto Encyclopedia of Genes and Genomes (KEGG) terms, pathways in cancer, prostate cancer and RIG‑I‑like receptor signaling pathway, were identified as associated with miR‑193a‑5p in lung cancer. In addition, in lung cancer, six key miR‑193a‑5p target genes, receptor tyrosine‑protein kinase erbB‑2 (ERBB2), nuclear cap‑binding protein subunit 2 (NCBP2), collagen α‑1(I) chain (COL1A1), roprotein convertase subtilisin/kexin type 9 (PCSK9), casein kinase II subunit α (CSNK2A1) and nucleolar transcription factor 1 (UBTF), were identified, five of which were significantly upregulated (ERBB2, NCBP2, COL1A1, CSNK2A1 and UBTF). The protein expression of ERBB2, NCBP2, COL1A1, CSNK2A1 and UBTF was also upregulated. NCBP2 and CSNK2A1 were negatively correlated with miR‑193a‑5p. The results demonstrated that miR‑193a‑5p exhibited opposite expression patterns in peripheral blood and tissue. Upregulated peripheral blood miR‑193a‑5p and downregulated tissue miR‑193a‑5p may be promising diagnostic biomarkers in lung cancer. In addition, the KEGG terms pathways in cancer, prostate cancer and RIG‑I‑like receptor signaling pathway may suggest which pathways serve vital roles in lung cancer by regulating miR‑193a‑5p. In addition, six genes, ERBB2, COL1A1, PCSK9, UBTF and particularly NCBP2 and CSNK2A1, may be key target genes of miR‑193a‑5p in lung cancer.
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October-2018
Volume 16 Issue 4

Print ISSN: 1792-1074
Online ISSN:1792-1082

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  • CiteScore: 5.7
  • CiteScore Rank: Q2: #139/404 Oncology
  • Source Normalized Impact per Paper (SNIP): 0.574
  • SCImago Journal Rank (SJR): 0.644
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Spandidos Publications style
Xie ZC, Tang RX, Gao X, Xie QN, Lin JY, Chen G and Li ZY: A meta‑analysis and bioinformatics exploration of the diagnostic value and molecular mechanism of miR‑193a‑5p in lung cancer. Oncol Lett 16: 4114-4128, 2018.
APA
Xie, Z., Tang, R., Gao, X., Xie, Q., Lin, J., Chen, G., & Li, Z. (2018). A meta‑analysis and bioinformatics exploration of the diagnostic value and molecular mechanism of miR‑193a‑5p in lung cancer. Oncology Letters, 16, 4114-4128. https://doi.org/10.3892/ol.2018.9174
MLA
Xie, Z., Tang, R., Gao, X., Xie, Q., Lin, J., Chen, G., Li, Z."A meta‑analysis and bioinformatics exploration of the diagnostic value and molecular mechanism of miR‑193a‑5p in lung cancer". Oncology Letters 16.4 (2018): 4114-4128.
Chicago
Xie, Z., Tang, R., Gao, X., Xie, Q., Lin, J., Chen, G., Li, Z."A meta‑analysis and bioinformatics exploration of the diagnostic value and molecular mechanism of miR‑193a‑5p in lung cancer". Oncology Letters 16, no. 4 (2018): 4114-4128. https://doi.org/10.3892/ol.2018.9174