Role of microRNA-4458 in patients with non-small-cell lung cancer

  • Authors:
    • Lidao Bao
    • Linlin Wang
    • Guomin Wei
    • Yuehong Wang
    • Gerile Wuyun
    • Agula Bo
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  • Published online on: September 22, 2016     https://doi.org/10.3892/ol.2016.5176
  • Pages: 3958-3966
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Abstract

Incidence and progression of non-small-cell lung cancer (NSCLC) is a multi-factor, multi-step process. The present study investigated the association between the expression level of microRNA (miR)‑4458 in NSCLC and paracarcinoma liver tissues and survival rates, and studied the biological functions of miR‑4458 at the cellular and protein level. NSCLC and paracarcinoma tissues were sequenced using a miR expression chip. The association between miR‑4458 expression and tumor‑node‑metastasis staging, total survival rate and relapse‑free survival rate was analyzed. miR‑4458 was subjected to target gene prediction. The target protein of cyclin D1 (CCND1) was verified with western blot analysis, immunohistochemistry and a luciferase reporter assay. The relative level of miR‑4458 in paracarcinoma tissues of 9 NSCLC patients decreased from 2.38 to 0.65 (P<0.001). Total five‑year survival rates of the high‑expression miR‑4458 group (29.21%) significantly exceeded that of the low‑expression group (14.37%) (P=0.025). The viability of human lung carcinoma A549 and H460 cells transfected with miR‑4458 decreased significantly compared with cells transfected with a normal control (blank control plasmid) within 72 h (P<0.001). The percentage of A549 and H460 cells transfected with a miR‑4458 mimic at the cell cycle stage G0/G1 was 69.94±8.05 and 68.15±7.75%, respectively. The percentages increased significantly compared with the control group (46.06±6.93 for A549 cells; 45.22±7.24 for H640 cells; P<0.001). CCND1 mRNA was downregulated significantly in H460 cells 72 h subsequent to the addition of miR‑4458 mimics (P<0.001). The activity of mutant‑CCND1 altered slightly, while the fluorescence intensity of the wild‑type‑CCND1 group decreased significantly following the addition of miR‑4458 mimics. In conclusion, miR‑4458 was expressed at low levels in lung cancer tissues, and it arrested cells in vitro at stage G0/G1 and inhibited cell proliferation. Therefore, miR‑4458 may participate in the onset of lung cancer as a suppressor gene by inhibiting CCND1.
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November-2016
Volume 12 Issue 5

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

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Copy and paste a formatted citation
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Spandidos Publications style
Bao L, Wang L, Wei G, Wang Y, Wuyun G and Bo A: Role of microRNA-4458 in patients with non-small-cell lung cancer. Oncol Lett 12: 3958-3966, 2016
APA
Bao, L., Wang, L., Wei, G., Wang, Y., Wuyun, G., & Bo, A. (2016). Role of microRNA-4458 in patients with non-small-cell lung cancer. Oncology Letters, 12, 3958-3966. https://doi.org/10.3892/ol.2016.5176
MLA
Bao, L., Wang, L., Wei, G., Wang, Y., Wuyun, G., Bo, A."Role of microRNA-4458 in patients with non-small-cell lung cancer". Oncology Letters 12.5 (2016): 3958-3966.
Chicago
Bao, L., Wang, L., Wei, G., Wang, Y., Wuyun, G., Bo, A."Role of microRNA-4458 in patients with non-small-cell lung cancer". Oncology Letters 12, no. 5 (2016): 3958-3966. https://doi.org/10.3892/ol.2016.5176