MicroRNA-34a: a potential therapeutic target in human cancer

Li, X J; Zhao, Rongjun; Tang, Jie

doi:10.1038/cddis.2014.270

Cited by 245 publications

(225 citation statements)

References 89 publications

(106 reference statements)

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“…The results were similar to observations in colon, breast and lung cancer, in which miR-34a expression was downregulated, and overexpression of miR-34a inhibited cell proliferation (7,26,27). The present study selected SIRT1, an energy sensor, to validate the antitumor mechanism of miR-34a in prostate cancer cells.…”

Section: Discussionsupporting

confidence: 70%

“…These results indicated that dysregulation of miR-34a may be involved in the pathogenesis of human prostate cancer. miR-34a is located on chromosome 1p-36; deletion or loss of heterozygosity of this region is associated with a number of types of human tumor, including breast cancer, lung cancer and cervical cancer (7). In addition, miR-34a is the target gene of the p53 tumor suppressor gene, and p53 tumor suppressor gene mutation is involved in the development of prostate cancer (21).…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence indicate that miRNAs are important regulatory molecules in various biological processes, including cell differentiation, proliferation, apoptosis and metabolism (6). miR-34a is located on chromosome 1p-36.23 in humans and highly expressed in multiple types of cancer such as colon cancer and lung cancer (7). The tumor suppressor protein p53 induces transcription of miR-34a and the expression of miR-34a correlates well with activation of p53 by genotoxic stress activation (8).…”

Section: Introductionmentioning

confidence: 99%

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miR-34a inhibits cell proliferation in prostate cancer by downregulation of SIRT1 expression

Duan

Zhang

et al. 2015

Oncology Letters

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Abstract. MicroRNA-34a (miR-34a) functions as a tumor suppressor gene and inhibits abnormal cell growth by regulating the expression of other genes. The role of miR-34a in regulating sirtuin 1 (SIRT1) in prostate cancer remains unclear. The objective of the present study was to investigate the biological function and molecular mechanisms of miR-34a regulation of SIRT1 in human prostate cancer samples and the human prostate cancer cell line, PC-3. Fresh prostate tissues were obtained from patients, and the miR-34a expression in prostate cancer tissues was measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). qPCR and western blotting were performed to assess the effects of miR-34a overexpression on SIRT1 regulation in PC-3 cells, and the cell growth was assessed by Cell Counting Kit-8 (CCK-8). Flow cytometry was used to assess the cell cycle status of the cells. The miR-34a expression levels in prostate cancer tissues were significantly reduced compared with adjacent normal prostate tissues (P<0.05). SIRT1 expression levels in PC-3 cells with over-expression of miR-34a were significantly reduced compared with those in the negative control (P<0.05). The over-expression of miR-34a inhibited PC-3 cells growth and resulted in increased cell cycle arrest compared with the negative control (P<0.05). In conclusion, miR-34a inhibits the human prostate cancer cell proliferation, in part, through the downregulation of SIRT1 expression.

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR-34a inhibits cell proliferation in prostate cancer by downregulation of SIRT1 expression

Duan

Zhang

et al. 2015

Oncology Letters

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“…The miR-34 family, including miR-34a, miR-34b and miR-34c, is directly regulated by p53 and has been reported to induce apoptosis and cell cycle arrest and, thus, act as a tumor suppressor in cancer cells (81). As was expected, low expression of miR-34a has also been found to be important in GBC (82).…”

Section: Tumor Suppressor Micrornassupporting

confidence: 54%

The role of microRNAs in gallbladder cancer

Yang

Zhang

et al. 2016

Molecular and Clinical Oncology

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Abstract. MicroRNAs (also referred to as miRNAs or miRs) play a crucial role in post-transcriptional gene regulation and serve as negative gene regulators by controlling a variety of target genes and regulating diverse biological processes, such as cell proliferation, invasion, migration and apoptosis. Aberrant expression of miRNAs is associated with the development and progression of cancer. Recent studies have reported that miRNAs may repress or promote the expression of cancer-related genes via several different signaling pathways in gallbladder cancer (GBC) patients and may function as tumor suppressors or oncogenes, thus providing a promising tool for the diagnosis and therapeutics of GBCs. In this review, we summarize the role of dysregulawted miRNA expression in the signaling pathways implicated in GBC and discuss the significant role of circulating miRNAs in GBC. Therefore, miRNAs may serve as novel therapeutic targets as well as diagnostic or prognostic markers in GBC.

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“…[35][36][37][38] Furthermore, it has been reported that miR-34 decreased the expression of Bcl-2, leading to an increase in apoptosis. 39 As one of the key regulators of apoptosis and autophagy, Bcl-2 protein possesses four conserved Bcl-2 homology domains (BH1-4) and can inhibit Beclin1-dependent autophagy by binding to Beclin1 under starvation conditions.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of B-cell lymphoma/leukemia-2 by overexpressed microRNA 34a enhanced titanium dioxide nanoparticle-induced autophagy in BEAS-2B cells

Bai¹,

Chen²,

Sun³

et al. 2016

IJN

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Titanium dioxide (TiO 2 ) nanoparticles (TNPs) are manufactured worldwide for a wide range of applications and the toxic effect of TNPs on biological systems is gaining attention. Autophagy is recognized as an emerging toxicity mechanism triggered by nanomaterials. MicroRNA 34a (miR34a) acts as a tumor suppressor gene by targeting many oncogenes, but how it affects autophagy induced by TNPs is not completely understood. Here, we observed the activation of TNP-induced autophagy through monodansylcadaverine staining and LC3-I/LC3-II conversion. Meanwhile, the transmission electron microscope ultrastructural analysis showed typical morphological characteristics in autophagy process. We detected the expression of miR34a and B-cell lymphoma/leukemia-2 (Bcl-2). In addition, the underlying mechanism of TNP-induced autophagy was performed using overexpression of miR34a by lentivirus vector transfection. Results showed that TNPs induced autophagy generation evidently. Typical morphological changes in the process of autophagy were observed by the transmission electron microscope ultrastructural analysis and LC3-I/LC3-II conversion increased significantly in TNP-treated cells. Meanwhile, TNPs induced the downregulation of miR34a and increased the expression of Bcl-2. Furthermore, overexpressed miR34a decreased the expression of Bcl-2 both in messenger RNA and protein level, following which the level of autophagy and cell death rate increased after the transfected cells were incubated with TNPs for 24 hours. These findings provide the first evidence that overexpressed miR34a enhanced TNP-induced autophagy and cell death through targeted downregulation of Bcl-2 in BEAS-2B cells.

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MicroRNA-34a: a potential therapeutic target in human cancer

Cited by 245 publications

References 89 publications

miR-34a inhibits cell proliferation in prostate cancer by downregulation of SIRT1 expression

miR-34a inhibits cell proliferation in prostate cancer by downregulation of SIRT1 expression

The role of microRNAs in gallbladder cancer

Downregulation of B-cell lymphoma/leukemia-2 by overexpressed microRNA 34a enhanced titanium dioxide nanoparticle-induced autophagy in BEAS-2B cells

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