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Effects of mdig on proliferation and apoptosis of lung cancer cells

  • Authors:
    • Xiaohui Xu
    • Lei Cao
    • Ye Zhang
    • Hongjian Lian
    • Zhiwei Sun
    • Yushang Cui
  • View Affiliations / Copyright

    Affiliations: Department of Thoracic Surgery, Peking Union Medical College Hospital, Beijing 100730, P.R. China
    Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 7146-7151
    |
    Published online on: September 28, 2018
       https://doi.org/10.3892/ol.2018.9528
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Abstract

Expression of mineral dust-induced gene (mdig) in lung cancer NCI-H1650 cells was detected to investigate the effects of mdig on proliferation and apoptosis of NCI‑H1650 cells. NCI‑H1650 lung cancer cells were cultured in vitro. The expression of mdig in NCI‑H1650 cells was lowered using ribonucleic acid interference (RNAi) technique. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were used to detect the effects of mdig small interfering RNA (siRNA) on messenger RNA (mRNA) and the protein expression of mdig in lung cancer NCI‑H1650 cells, respectively. The effect of mdig on the proliferation of NCI‑H1650 cells was observed through 3-(4,5)-dimethylthiazol (-z-y1)-3,5-di-phenyl tetrazolium bromide (MTT) assay, and flow cytometry was used to detect the impact of mdig on cell cycle and apoptosis of NCI‑H1650 cells. The influence of mdig on caspase‑3 and poly (ADP-ribose) polymerase 1 (PARP1) proteins in NCI‑H1650 cells were investigated via western blot analysis. The results of RT-qPCR and western blot analysis showed that mdig siRNA obviously inhibited the expression of mRNA and protein of mdig in NCI‑H1650 cells. Results of the MTT assay showed mdig siRNA could significantly reduce the proliferation ability of NCI‑H1650 cells. In addition cell cycle detection showed that mdig siRNA caused NCI‑H1650 cell arrest at G1 phase. Apoptosis detection results indicated that mdig siRNA promoted apoptosis of NCI‑H1650 cells. Western-blot analysis revealed that mdig siRNA upregulated the expression of cleaved caspase‑3 and cleaved PARP1 proteins in NCI‑H1650 cells. Mdig is highly expressed in lung cancer NCI‑H1650 cells while mdig siRNA can inhibit proliferation of NCI‑H1650 cells and accelerate apoptosis. The underlying mechanism may be related to inhibited cell cycle progression and upregulated expression of cleavage proteins (cleaved caspase‑3 and cleaved PARP1).
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Copy and paste a formatted citation
Spandidos Publications style
Xu X, Cao L, Zhang Y, Lian H, Sun Z and Cui Y: Effects of mdig on proliferation and apoptosis of lung cancer cells. Oncol Lett 16: 7146-7151, 2018.
APA
Xu, X., Cao, L., Zhang, Y., Lian, H., Sun, Z., & Cui, Y. (2018). Effects of mdig on proliferation and apoptosis of lung cancer cells. Oncology Letters, 16, 7146-7151. https://doi.org/10.3892/ol.2018.9528
MLA
Xu, X., Cao, L., Zhang, Y., Lian, H., Sun, Z., Cui, Y."Effects of mdig on proliferation and apoptosis of lung cancer cells". Oncology Letters 16.6 (2018): 7146-7151.
Chicago
Xu, X., Cao, L., Zhang, Y., Lian, H., Sun, Z., Cui, Y."Effects of mdig on proliferation and apoptosis of lung cancer cells". Oncology Letters 16, no. 6 (2018): 7146-7151. https://doi.org/10.3892/ol.2018.9528
Copy and paste a formatted citation
x
Spandidos Publications style
Xu X, Cao L, Zhang Y, Lian H, Sun Z and Cui Y: Effects of mdig on proliferation and apoptosis of lung cancer cells. Oncol Lett 16: 7146-7151, 2018.
APA
Xu, X., Cao, L., Zhang, Y., Lian, H., Sun, Z., & Cui, Y. (2018). Effects of mdig on proliferation and apoptosis of lung cancer cells. Oncology Letters, 16, 7146-7151. https://doi.org/10.3892/ol.2018.9528
MLA
Xu, X., Cao, L., Zhang, Y., Lian, H., Sun, Z., Cui, Y."Effects of mdig on proliferation and apoptosis of lung cancer cells". Oncology Letters 16.6 (2018): 7146-7151.
Chicago
Xu, X., Cao, L., Zhang, Y., Lian, H., Sun, Z., Cui, Y."Effects of mdig on proliferation and apoptosis of lung cancer cells". Oncology Letters 16, no. 6 (2018): 7146-7151. https://doi.org/10.3892/ol.2018.9528
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