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Downregulation of miR-329 promotes cell invasion by regulating BRD4 and predicts poor prognosis in hepatocellular carcinoma

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Tumor Biology

Abstract

Increasing evidence indicates that abnormal microRNA (miRNA) expression is related to hepatocellular carcinoma (HCC) development. Our study aimed to elucidate the essential role of miR-329 in HCC progression. Real-time PCR was used to analyze miR-329 and bromodomain containing 4 (BRD4) expression in HCC samples (n = 135). Cell Counting Kit-8 (CCK-8) and flow cytometric analysis were used to investigate cell proliferation and apoptosis. The transwell assay was used to examine the cell invasive ability. The regulation mechanism was confirmed by luciferase reporter and western blot assays. Kaplan-Meier analysis was used to detect the function of miR-329 on the prognosis of HCC patients. miR-329 was decreased in HCC samples and was related to tumor development. Furthermore, miR-329 significantly regulated cell invasion by targeting BRD4 but had no effect on cell proliferation and apoptosis. Moreover, downregulation of miR-329 predicted poor prognosis of HCC patients. miR-329 could control cell invasion via regulating BRD4 expression and may be a prognostic marker in HCC.

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Abbreviations

BRD4:

Bromodomain containing 4

HCC:

Hepatocellular carcinoma

UTR:

Untranslated region

siRNA:

Small interfering RNA

CCK-8:

Cell Counting Kit-8

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Acknowledgments

Thanks to Dr. Junwei Tang (The First Affiliated Hospital of Nanjing Medical University, Nanjing, China) for providing the HCC samples and cell lines.

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The informed consent approval from The First Affiliated Hospital of Nanjing Medical University Institute Research Ethics Committee was obtained.

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Correspondence to Jiangang Zhou.

Additional information

Jianping Zhou and Weiling Li contributed equally to this work.

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Zhou, J., Li, W., Guo, J. et al. Downregulation of miR-329 promotes cell invasion by regulating BRD4 and predicts poor prognosis in hepatocellular carcinoma. Tumor Biol. 37, 3561–3569 (2016). https://doi.org/10.1007/s13277-015-4109-4

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  • DOI: https://doi.org/10.1007/s13277-015-4109-4

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