Dysregulated microRNA-224/apelin axis associated with aggressive progression and poor prognosis in patients with prostate cancer
Summary Our previous study revealed that microRNA (miR)-224 down-regulation could promote tumor progression of prostate cancer (PCa) and might be associated with poor biochemical recurrence–free survival of patients with this malignancy. However, the underlying mechanisms of miR-224 have not been fu...
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Veröffentlicht in: | Human pathology 2015-02, Vol.46 (2), p.295-303 |
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Sprache: | eng |
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Zusammenfassung: | Summary Our previous study revealed that microRNA (miR)-224 down-regulation could promote tumor progression of prostate cancer (PCa) and might be associated with poor biochemical recurrence–free survival of patients with this malignancy. However, the underlying mechanisms of miR-224 have not been fully elucidated. In the current study, apelin ( APLN ) was identified as a target gene of miR-224. Forced expression of miR-224 inhibited PCa cell invasion and migration by suppressing the expression of APLN. In addition, the down-regulation of miR-224 was negatively correlated with the up-regulation of APLN mRNA in PCa tissues. Moreover, miR-224 down-regulation was significantly associated with advanced clinical stage ( P = .027) and metastasis ( P = .001), whereas APLN up-regulation more frequently occurred in PCa tissues with advanced pathologic stage ( P = .003), metastasis ( P < .001), and prostate-specific antigen failure ( P = .001). Furthermore, patients with PCa in the miR-224–low/APLN-high group more frequently had shorter biochemical recurrence–free survival than those in groups with other expression patterns of the 2 molecules. Taken together, our data strongly confirmed for the first time that the dysregulated miR-224/APLN axis may be associated with tumorigenesis and aggressive progression of PCa. More importantly, miR-224 down-regulation and APLN up-regulation may synergistically predict biochemical recurrence–free survival in patients with PCa. |
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ISSN: | 0046-8177 1532-8392 |
DOI: | 10.1016/j.humpath.2014.10.027 |