A correlation analysis of miRNA-34a and its predicted target genes in leukemia

Tang, Ruihong; Li, Juanjuan; Yue, Mei; Liu, Ziqin; Feng, Shunqiao; Tang, Suo-Qin; Wang, Tianyou

doi:10.3892/mmr.2014.1931

Cited by 6 publications

(5 citation statements)

References 30 publications

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“…MYB is a well-acknowledged oncogene in several types of human cancer. Knockdown of MYB contributes to inhibit malignant transformation by regulating genes that participate in numerous aspects of tumorigenesis, including cell growth arrest, invasion inhibition and apoptosis induction (21)(22)(23)(24). In the present study, knockdown of MYB expression significantly decreased the proliferation and invasion of A172 and U87 cells, which was similar to the effects of hsa-miR-495 overexpression.…”

Section: Discussionsupporting

confidence: 78%

Hsa-miR-495 acts as a tumor suppressor gene in glioma via the negative regulation of MYB

Zhang

Yuan

Liu

et al. 2016

Molecular Medicine Reports

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MicroRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression at the post-transcriptional level. Previous studies have reported that there are causative links between the abnormal regulation of miRNAs and cancer development. Hsa‑miR‑495 has previously been demonstrated to be downregulated, and to function as a tumor suppressor, in numerous types of human cancer. However, the function and molecular mechanism of hsa‑miR‑495 in glioma remains unclear. In the current study, the expression and effects of hsa‑miR‑495 on glioma were evaluated. It was identified that the expression levels of hsa-miR-495 were downregulated in glioma tissues and cell lines. Furthermore, restoration of hsa-miR-495 inhibited glioma cell proliferation and invasion in vitro. Notably, a luciferase reporter assay revealed that hsa‑miR‑495 was able to directly target v‑myb avian myeloblastosis viral oncogene homolog (MYB) in glioma cells. In addition, an RNA interference assay indicated that MYB knockdown inhibited glioma cell proliferation and invasion in vitro. In conclusion, the results of the present study suggested that hsa‑miR‑495 may act as a tumor suppressor gene in glioma by directly inhibiting MYB expression, which may provide a novel therapeutic strategy for the treatment of glioma.

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Section: Discussionsupporting

confidence: 78%

Hsa-miR-495 acts as a tumor suppressor gene in glioma via the negative regulation of MYB

Zhang

Yuan

Liu

et al. 2016

Molecular Medicine Reports

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“…Other targets of miR‐34a have also been revealed. MicroRNA‐34a is negatively correlated with CDK4, Sirt1 and myeloblastosis protein . In cell biology, miRNA‐34a has been associated with hypoxia increased epithelial‐mesenchymal transition and docetaxel resistance in breast cancer .…”

Section: Human Papillomavirus E6 Proteinmentioning

confidence: 99%

Signaling pathways in HPV‐associated cancers and therapeutic implications

Chen

2015

Reviews in Medical Virology

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Human papillomaviruses (HPVs) are small double-stranded circular DNA viruses with 8 kb genomes. So far, more than 150 HPVs have been identified, and 12 types of HPVs have been conclusively linked to cancer by the International Agency for Research on Cancer/World Health Organization. Expression of HPV E5, E6 and E7 oncoproteins can alter multiple signaling pathways to cause cancer. In this review, the signaling pathways activated by these oncoproteins are summarized, and targeted therapy against key signaling molecules is described. E6 can inactivate tumor protein 53 and PDZ (post synaptic density protein-drosophila disk large tumor suppressor-zonula occludens-1 proteins) while stimulating phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), Wnt and Notch pathways. E7 can inhibit retinoblastoma protein and stimulate the PI3K/Akt pathway. Both E6 and E7 can deregulate cellular microRNA expression, which can alter cellular signaling pathways. E5 can sensitize epidermal growth factor receptor to epidermal growth factor to increase activation of PI3K/Akt and mitogen-activated protein kinase pathways. E5 can also inhibit the extrinsic apoptotic pathway. These altered signaling pathways could be critical for the initiation and maintenance of HPVassociated cancers. Therefore, targeted therapy against the key signaling molecules has therapeutic implications. Among these, the possibilities of targeting PI3K/Akt, mammalian target of rapamycin, epidermal growth factor receptor and vascular endothelial growth factor have been extensively studied in many cancers. Some inhibitors have been studied in cervical cancer in both animal models and clinical trials. Although the results are promising, further investigation is warranted.

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“…Referring to previous studies [24, 25] and using a target prediction and validation program, miRWalk 2.0 [26], we chose 7 potential target genes of miR34a to examine further in AA patients and healthy individuals. These genes included Kruppel-like factor 4 (KLF4), lymphoid enhancer binding factor 1 (LEF1), SPI-1 proto-oncogene (SPI1), nuclear receptor subfamily 4 group A member 2 (NR4A2), sirtuin 1 (SIRT1), cyclin-dependent kinase 6 (CDK6), and DGKζ.…”

Section: Resultsmentioning

confidence: 99%

“…In some hematological malignancies, miR34a is dysregulated and plays a role in the pathogenesis by repressing its target genes, such as SIRT1 and FOXP1 [24, 30]. Unlike miR155 and miR146, which have been reported to be aberrantly expressed in many autoimmune diseases [31], little has been reported regarding miR34a.…”

Section: Discussionmentioning

confidence: 99%

Dysregulated miR34a/diacylglycerol kinase ζ interaction enhances T-cell activation in acquired aplastic anemia

Sun

Feng

et al. 2016

Oncotarget

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Acquired aplastic anemia is an idiopathic paradigm of human bone marrow failure syndrome, which involves active destruction of hematopoietic stem cells and progenitors by cytotoxic T cells in the bone marrow. Aberrant expression of microRNAs in T cells has been shown to lead to development of certain autoimmune diseases. In the present study, we performed a microarray analysis of miRNA expression in bone marrow CD3+ T cells from patients with aplastic anemia and healthy controls. Overexpression of miR34a and underexpression of its target gene diacylglycerol kinase (DGK) ζ in bone marrow mononuclear cells were validated in 41 patients and associated with the severity of aplastic anemia. Further, the level of miR34a was higher in naïve T cells from patients than from controls. The role of miR34a and DGKζ in aplastic anemia was investigated in a murine model of immune-mediated bone marrow failure using miR34a−/− mice. After T-cell receptor stimulation in vitro, lymph node T cells from miR34a−/− mice demonstrated reduced activation and proliferation accompanied with a less profound down-regulation of DGKζ expression and decreased ERK phosphorylation compared to those from wild-type C57BL6 control mice. Infusion of 5 × 106 miR34a−/− lymph node T cells into sublethally irradiated CB6F1 recipients led to increased Lin-Sca1+CD117+ cells and less vigorous expansion of CD8+ T cells than injection of same number of wild-type lymph node cells. Our study demonstrates that the miR34a/DGKζ dysregulation enhances T-cell activation in aplastic anemia and targeting miR34a may represent a novel molecular therapeutic approach for patients with aplastic anemia.

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A correlation analysis of miRNA-34a and its predicted target genes in leukemia

Cited by 6 publications

References 30 publications

Hsa-miR-495 acts as a tumor suppressor gene in glioma via the negative regulation of MYB

Hsa-miR-495 acts as a tumor suppressor gene in glioma via the negative regulation of MYB

Signaling pathways in HPV‐associated cancers and therapeutic implications

Dysregulated miR34a/diacylglycerol kinase ζ interaction enhances T-cell activation in acquired aplastic anemia

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