SIRT3 is correlated with the malignancy of non-small cell lung cancer

  • Authors:
    • Yanlu Xiong
    • Mingxing Wang
    • Jinbo Zhao
    • Lei Wang
    • Xiaofei Li
    • Zhipei Zhang
    • Lintao Jia
    • Yong Han
  • View Affiliations

  • Published online on: February 2, 2017     https://doi.org/10.3892/ijo.2017.3868
  • Pages: 903-910
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Abstract

The mitochondrial deacetylase SIRT3 plays a pivotal role in the initiation and the progression of certain cancers acting as an oncogene. However, in others it acts anti-oncogenically. Its conflicting action is possibly due to the different key proteins it modifies depending on the context of active intracellular signaling pathways in different cancers. SIRT3 is thus a novel target for preventing and treating cancer. In the present study, we explored the function of SIRT3 in non-small cell lung cancer (NSCLC) with the aim of elucidating the underlying mechanisms. We first determined the SIRT3 expression levels by real-time PCR, western blotting and immunohistochemistry on tissue microarrays of paired samples of NSCLC tissue and adjacent normal tissue from 70 patients with associated clinicopathological data. Levels of SIRT3 protein and mRNA were significantly increased in NSCLC tissue, compared with normal tissue (P<0.05). Expression of SIRT3 in NSCLC positively correlated with that of malignant biomarker Ki-67 (P<0.05) and oncogene p-Akt (P<0.05). Patients with higher SIRT3 expression had a shorter overall survival duration (P<0.05). NSCLC tissue of squamous cell carcinoma type had higher SIRT3 expression compared with other types (P<0.05). Furthermore, among the clinicopathological variables examined, SIRT3 expression was correlated only with pathological type (P<0.05). In NSCLC cell lines, we found that downregulation of SIRT3 by siRNA decreased the activation of Akt, and that SIRT3 overexpression caused the activation of Akt. In addition, in a NSCLC cell line, SIRT3 was able to co-immunoprecipitate Akt and co-located with Akt, suggesting that SIRT3 regulates the activation of Akt through post-transcriptional modification. Our findings suggest that SIRT3 promotes the malignancy of NSCLC, showing an oncogenic preference towards squamous cell carcinoma, and that could represent a novel target for treatment.
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March-2017
Volume 50 Issue 3

Print ISSN: 1019-6439
Online ISSN:1791-2423

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Spandidos Publications style
Xiong Y, Wang M, Zhao J, Wang L, Li X, Zhang Z, Jia L and Han Y: SIRT3 is correlated with the malignancy of non-small cell lung cancer. Int J Oncol 50: 903-910, 2017
APA
Xiong, Y., Wang, M., Zhao, J., Wang, L., Li, X., Zhang, Z. ... Han, Y. (2017). SIRT3 is correlated with the malignancy of non-small cell lung cancer. International Journal of Oncology, 50, 903-910. https://doi.org/10.3892/ijo.2017.3868
MLA
Xiong, Y., Wang, M., Zhao, J., Wang, L., Li, X., Zhang, Z., Jia, L., Han, Y."SIRT3 is correlated with the malignancy of non-small cell lung cancer". International Journal of Oncology 50.3 (2017): 903-910.
Chicago
Xiong, Y., Wang, M., Zhao, J., Wang, L., Li, X., Zhang, Z., Jia, L., Han, Y."SIRT3 is correlated with the malignancy of non-small cell lung cancer". International Journal of Oncology 50, no. 3 (2017): 903-910. https://doi.org/10.3892/ijo.2017.3868