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2014-February Volume 7 Issue 2

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International Journal of Molecular Medicine

International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

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International Journal of Oncology is an international journal devoted to oncology research and cancer treatment.

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Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.

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Oncology Reports is an international journal devoted to fundamental and applied research in Oncology.

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Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine.

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Oncology Letters is an international journal devoted to Experimental and Clinical Oncology.

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Article

miR‑101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3‑dependent apoptosis

  • Authors:
    • Jiqing Yin
    • Mingguo Wang
    • Cuixiang Jin
    • Qingguo Qi
  • View Affiliations / Copyright

    Affiliations: Department of General Practice, Shandong University Hospital, Jinan, Shandong 250061, P.R. China, Department of Stomatology, Subsidiary Central Hospital, Shandong University, Jinan, Shandong 250061, P.R. China, Department of Stomatology, Stomatology Hospital of Shandong University, Jinan, Shandong 250061, P.R. China
  • Pages: 461-465
    |
    Published online on: December 3, 2013
       https://doi.org/10.3892/ol.2013.1725
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Abstract

MicroRNA‑101 (miR‑101) is evidently downregulated in several types of cancer, including non‑small cell lung cancer (NSCLC), and is crucial in sensitizing cells to chemotherapy drugs. The aim of the present study was to investigate the correlation between miR‑101 and chemosensitivity in the A549 NSCLC cell line. Here, we used the human A549 cell line for transfection with an miR-101 overexpressing vector and detected the cytotoxic acticity, proliferation and apoptosis of cis‑diaminedichloroplatinum (CDDP) in A549-miR-101 and A549-mock cells. We demonstrated that overexpression of miR‑101 sensitized A549 cells to CDDP, one of the most frequently used agents in curing or controlling NSCLC and enhanced CDDP‑induced cell death and caspase 3‑dependent apoptosis. In addition, miR‑101 facilitated the inhibitory role of CDDP in A549 cell colony formation. Overall, the results of the present study demonstrated that miR‑101 sensitizes the A549 NSCLC cell line to CDDP via the activation of caspase 3‑dependent apoptosis.
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Copy and paste a formatted citation
Spandidos Publications style
Yin J, Wang M, Jin C and Qi Q: miR‑101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3‑dependent apoptosis. Oncol Lett 7: 461-465, 2014.
APA
Yin, J., Wang, M., Jin, C., & Qi, Q. (2014). miR‑101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3‑dependent apoptosis. Oncology Letters, 7, 461-465. https://doi.org/10.3892/ol.2013.1725
MLA
Yin, J., Wang, M., Jin, C., Qi, Q."miR‑101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3‑dependent apoptosis". Oncology Letters 7.2 (2014): 461-465.
Chicago
Yin, J., Wang, M., Jin, C., Qi, Q."miR‑101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3‑dependent apoptosis". Oncology Letters 7, no. 2 (2014): 461-465. https://doi.org/10.3892/ol.2013.1725
Copy and paste a formatted citation
x
Spandidos Publications style
Yin J, Wang M, Jin C and Qi Q: miR‑101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3‑dependent apoptosis. Oncol Lett 7: 461-465, 2014.
APA
Yin, J., Wang, M., Jin, C., & Qi, Q. (2014). miR‑101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3‑dependent apoptosis. Oncology Letters, 7, 461-465. https://doi.org/10.3892/ol.2013.1725
MLA
Yin, J., Wang, M., Jin, C., Qi, Q."miR‑101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3‑dependent apoptosis". Oncology Letters 7.2 (2014): 461-465.
Chicago
Yin, J., Wang, M., Jin, C., Qi, Q."miR‑101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3‑dependent apoptosis". Oncology Letters 7, no. 2 (2014): 461-465. https://doi.org/10.3892/ol.2013.1725
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