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miR‑101‑3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5

  • Authors:
    • Xin Meng
    • Yanfei Sun
    • Shiying Liu
    • Yanchao Mu
  • View Affiliations / Copyright

    Affiliations: Department of Hyperbaric Oxygen, The First Affiliated Hospital of China Medical University, Liaoning, Shenyang 110001, P.R. China, Trauma Center/Burn Ward, The First Affiliated Hospital of China Medical University, Liaoning, Shenyang 110001, P.R. China, School of Nursing, China Medical University, Liaoning, Shenyang 110001, P.R. China, Department of Laboratory Medicine, Anyang Maternity and Child Healthcare Hospital, Anyang, Henan 455000, P.R. China
    Copyright: © Meng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 282
    |
    Published online on: February 10, 2021
       https://doi.org/10.3892/ol.2021.12543
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Abstract

Lung adenocarcinoma (LUAD) has been considered as the most common cause of cancer‑associated mortality. Radiotherapy resistance is one of the main reasons for LUAD treatment failure. The microRNA (miR)‑101‑3p has been previously reported to function as a tumor suppressor in several types of cancer, including LUAD. The present study aimed to explore the role and mechanism of miR‑101‑3p on radioresistance of lung adenocarcinoma cells through bioinformatics analysis and biological experiments. Based on the analysis of Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) data, it was demonstrated that the expression of miR‑101‑3p was low in LUAD tissues compared with normal lung tissues and was associated with poor prognosis of patients with LUAD. The results of the CCK‑8 assay, colony formation assay, immunofluorescence staining, caspase‑3 activity assay and western blotting demonstrated that miR‑101‑3p overexpression sensitized LUAD cells to ionizing radiation by decreasing the abilities of LUAD cell proliferation, colony formation, DNA damage repair and increasing caspase‑3 activity and apoptosis of LUAD cells following ionizing radiation. Furthermore, according to bioinformatics analysis and luciferase assay, baculoviral IAP repeat containing 5 (BIRC5) was identified as a direct target of miR‑101‑3p. Increased BIRC5 expression reversed the miR‑101‑3p‑mediated increase in LUAD cell radiotherapy sensitivity. Taken together, the results of the present study demonstrated that miR‑101‑3p may be considered as a potential target that can enhance LUAD cell sensitivity to radiotherapy, which may provide a new strategy to improve therapy in patients with LUAD.
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Copy and paste a formatted citation
Spandidos Publications style
Meng X, Sun Y, Liu S and Mu Y: miR‑101‑3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5. Oncol Lett 21: 282, 2021.
APA
Meng, X., Sun, Y., Liu, S., & Mu, Y. (2021). miR‑101‑3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5. Oncology Letters, 21, 282. https://doi.org/10.3892/ol.2021.12543
MLA
Meng, X., Sun, Y., Liu, S., Mu, Y."miR‑101‑3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5". Oncology Letters 21.4 (2021): 282.
Chicago
Meng, X., Sun, Y., Liu, S., Mu, Y."miR‑101‑3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5". Oncology Letters 21, no. 4 (2021): 282. https://doi.org/10.3892/ol.2021.12543
Copy and paste a formatted citation
x
Spandidos Publications style
Meng X, Sun Y, Liu S and Mu Y: miR‑101‑3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5. Oncol Lett 21: 282, 2021.
APA
Meng, X., Sun, Y., Liu, S., & Mu, Y. (2021). miR‑101‑3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5. Oncology Letters, 21, 282. https://doi.org/10.3892/ol.2021.12543
MLA
Meng, X., Sun, Y., Liu, S., Mu, Y."miR‑101‑3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5". Oncology Letters 21.4 (2021): 282.
Chicago
Meng, X., Sun, Y., Liu, S., Mu, Y."miR‑101‑3p sensitizes lung adenocarcinoma cells to irradiation via targeting BIRC5". Oncology Letters 21, no. 4 (2021): 282. https://doi.org/10.3892/ol.2021.12543
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