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Oncogenic miR‑744 promotes prostate cancer growth through direct targeting of LKB1

  • Authors:
    • Minglei Zhang
    • Hai Li
    • Yun Zhang
    • Hongyan Li

  • View Affiliations

  • Published online on: December 11, 2018     https://doi.org/10.3892/ol.2018.9822
  • Pages: 2257-2265

  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Prostate cancer (PCa) is one of the most common malignancies worldwide, and with a limited number of treatments for this type of cancer, its incidence is rapidly increasing. Patients presenting with PCa are likely to experience disease recurrence, which represents a considerable clinical challenge. MicroRNAs (miRNAs) have been widely characterized as a critical regulator in a number of types of cancer, including PCa. miRNA‑744 (miR‑744) has been reported to be involved in cancer regulation; however, its role in PCa remained poorly understood. In a recent study, it was demonstrated that miR‑744 was overexpressed in prostate tissue from PCa patients when compared with the surrounding tissues, and knockdown of miR‑744 resulted in reduced cell growth. In addition, an increased population of apoptotic cells was detected upon miR‑744 knockdown, together with a decrease in cell proliferation. Cell cycle analysis demonstrated a higher number of cells in the G1 phase and lower numbers in the S phase following miR‑744 silencing. The levels of key proteins involved in cell cycle progression (cyclin D1, cyclin‑dependent kinase 4, and proliferating cell nuclear antigen) were increased, whereas those proteins responsible for cell cycle inhibition (cyclin‑dependent kinase inhibitor p21) were decreased. The tumor suppressor liver kinase B1 (LKB1) was revealed to be a potential target of miR‑744, suggesting its potential mechanism of action. LKB1 levels were negatively correlated with miR‑744, and LKB1 was indicated to be a direct target of miR‑744. Furthermore, it was revealed that by targeting LKB1, miR‑744 may regulate adenosine monophosphate‑activated protein kinase (AMPK); the AMPK signaling pathway was activated by miR‑744 knockdown, with subsequent inhibition of the mammalian target of rapamycin (mTOR) signaling pathway. Taken together, these results demonstrated that miR‑744 promoted cell growth through the AMPK signaling pathway, by targeting LKB1. The present study revealed a novel insight into the biological function of miR‑744 in PCa, and that miR‑744 may be a potential therapeutic target.
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February-2019
Volume 17 Issue 2

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Zhang M, Li H, Zhang Y and Li H: Oncogenic miR‑744 promotes prostate cancer growth through direct targeting of LKB1. Oncol Lett 17: 2257-2265, 2019
APA
Zhang, M., Li, H., Zhang, Y., & Li, H. (2019). Oncogenic miR‑744 promotes prostate cancer growth through direct targeting of LKB1. Oncology Letters, 17, 2257-2265. https://doi.org/10.3892/ol.2018.9822
MLA
Zhang, M., Li, H., Zhang, Y., Li, H."Oncogenic miR‑744 promotes prostate cancer growth through direct targeting of LKB1". Oncology Letters 17.2 (2019): 2257-2265.
Chicago
Zhang, M., Li, H., Zhang, Y., Li, H."Oncogenic miR‑744 promotes prostate cancer growth through direct targeting of LKB1". Oncology Letters 17, no. 2 (2019): 2257-2265. https://doi.org/10.3892/ol.2018.9822