Open Access

MicroRNA‑3907 promotes the proliferation and migration of sebaceous gland carcinoma of the eyelid by targeting thrombospondin 1

  • Authors:
    • Chuanli Zhang
    • Limin Zhu
    • Xun Liu
    • Meixia Jiang
    • Qin Tang
    • Fei Xu
    • Tingting Lin
    • Lijie Dong
    • Yanjin He
  • View Affiliations

  • Published online on: October 14, 2021     https://doi.org/10.3892/ol.2021.13094
  • Article Number: 833
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

MicroRNAs (miRNAs/miRs) play an important role in various types of carcinoma, including sebaceous gland carcinoma (SGC) of the eyelid. miR‑3907 was found to be highly expressed in lung cancer; however, to the best of our knowledge, the biological role of miR‑3907 in SGC has not previously been evaluated. The aim of the present study was to determine the role and mechanism of miR‑3907 in the occurrence and development of SGC. miR‑3907 was screened and identified as a novel upregulated miRNA in SGC tissues and cells, as determined using miRNA microarrays and reverse transcription‑quantitative (RT‑q) PCR analyses. Compared with the control group, cellular proliferation and migration were enhanced in the miR‑3907 mimics group, and decreased in the miR‑3907 inhibitor group. Moreover, miR‑3907 negatively regulated thrombospondin 1 (THBS1) expression, as shown by bioinformatics prediction, RT‑qPCR, western blotting and dual‑luciferase reporter assays. In addition, compared with the control group, the small interfering (si) siRNA‑THBS1 group exhibited enhanced proliferation and migration abilities, which were decreased in the THBS1 overexpression group. Furthermore, THBS1 overexpression was found to attenuate the stimulative effect of miR‑3907 mimics, and THBS1‑knockdown reversed the inhibitory effect of the miR‑3907 inhibitor in SGC cells. Collectively, the results of the present study indicated that miR‑3907 promoted the proliferation and migration of SGC by downregulating THBS1, and that this axis may be a potential target for the prognostic assessment and treatment of SGC.
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