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Article

Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway

  • Authors:
    • Chaoxia Zou
    • Chendan Zou
    • Wanpeng Cheng
    • Qiang Li
    • Zhongjing Han
    • Xiaona Wang
    • Jianfeng Jin
    • Jiaqi Zou
    • Zhiyan Liu
    • Zhongqiu Zhou
    • Weiming Zhao
    • Zhimin Du
  • View Affiliations / Copyright

    Affiliations: Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, P.R. China, Department of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, P.R. China, Department of Hemopathology, General Hospital of Daqing Oil Field, Daqing, Heilongjiang, P.R. China, Institute of Clinical Pharmacy, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, P.R. China
  • Pages: 2715-2722
    |
    Published online on: August 30, 2016
       https://doi.org/10.3892/or.2016.5056
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Abstract

Heme metabolism system is involved in microRNA (miRNA) biogenesis. The complicated interplay between heme oxygenase-1 (HO-1) and miRNA has been observed in various tissues and diseases, including human malignancy. In the present study, our data showed that stable HO-1 overexpression in hepatocellular carcinoma (HCC) cells downregulated several oncomiRs. The most stably downregulated are miR-30d and miR-107. Iron, one of HO-1 catalytic products, was an important mediator in this regulation. Cell function analysis demonstrated that HO-1 inhibited the proliferation and metastasis of HepG2 cells, whereas miR-30d/miR-107 improved the proliferative and migratory ability of HepG2 cells. The beneficial effect of HO-1 in HCC inhibition could be reversed by upregulating miR-30d and miR-107. Akt and ERK pathways may be involved in the regulation of HO-1/miR-30d/miR-107 in HCC. These data indicate that HO-1 significantly suppresses HCC progression by regulating the miR-30d/miR-107 level, suggesting miR-30d/miR-107 regulation as a new molecular mechanism of HO-1 anticancer effect.
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Copy and paste a formatted citation
Spandidos Publications style
Zou C, Zou C, Cheng W, Li Q, Han Z, Wang X, Jin J, Zou J, Liu Z, Zhou Z, Zhou Z, et al: Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway. Oncol Rep 36: 2715-2722, 2016.
APA
Zou, C., Zou, C., Cheng, W., Li, Q., Han, Z., Wang, X. ... Du, Z. (2016). Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway. Oncology Reports, 36, 2715-2722. https://doi.org/10.3892/or.2016.5056
MLA
Zou, C., Zou, C., Cheng, W., Li, Q., Han, Z., Wang, X., Jin, J., Zou, J., Liu, Z., Zhou, Z., Zhao, W., Du, Z."Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway". Oncology Reports 36.5 (2016): 2715-2722.
Chicago
Zou, C., Zou, C., Cheng, W., Li, Q., Han, Z., Wang, X., Jin, J., Zou, J., Liu, Z., Zhou, Z., Zhao, W., Du, Z."Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway". Oncology Reports 36, no. 5 (2016): 2715-2722. https://doi.org/10.3892/or.2016.5056
Copy and paste a formatted citation
x
Spandidos Publications style
Zou C, Zou C, Cheng W, Li Q, Han Z, Wang X, Jin J, Zou J, Liu Z, Zhou Z, Zhou Z, et al: Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway. Oncol Rep 36: 2715-2722, 2016.
APA
Zou, C., Zou, C., Cheng, W., Li, Q., Han, Z., Wang, X. ... Du, Z. (2016). Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway. Oncology Reports, 36, 2715-2722. https://doi.org/10.3892/or.2016.5056
MLA
Zou, C., Zou, C., Cheng, W., Li, Q., Han, Z., Wang, X., Jin, J., Zou, J., Liu, Z., Zhou, Z., Zhao, W., Du, Z."Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway". Oncology Reports 36.5 (2016): 2715-2722.
Chicago
Zou, C., Zou, C., Cheng, W., Li, Q., Han, Z., Wang, X., Jin, J., Zou, J., Liu, Z., Zhou, Z., Zhao, W., Du, Z."Heme oxygenase-1 retards hepatocellular carcinoma progression through the microRNA pathway". Oncology Reports 36, no. 5 (2016): 2715-2722. https://doi.org/10.3892/or.2016.5056
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