microRNA-608 inhibits human hepatocellular carcinoma cell proliferation via targeting the BET family protein BRD4

He, Ling; Meng, Dong; Zhang, Shihu; Zhang, Yi; Deng, Zhangshuang; Kong, Lianbao

doi:10.1016/j.bbrc.2018.05.108

Cited by 19 publications

(11 citation statements)

References 28 publications

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“…He et al demonstrated that miR-608 could inhibit HCC cell proliferation possibly via targeting BET family protein BRD4. 19 miR-608, along with miR-342-5p can target NAA10 and inhibit colon cancer tumorigenesis. 20 Moreover, tumor-suppressive role of miR-608 has been found in lung adenocarcinoma 21 and bladder cancer.…”

Section: Introductionmentioning

confidence: 99%

<p>Toosendanin Suppresses Glioma Progression Property and Induces Apoptosis by Regulating miR-608/Notch Axis</p>

Wang

Hou

et al. 2020

CMAR

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Background: Glioma is one the most common and aggressive primary tumors of adult central nervous system worldwide, which tends to develop dysplasia and metastasis. Recently, toosendanin (TSN) has shown pharmacological effects in several cancers. However, little is known about the underlying mechanism of the effect of TSN on glioma and its relationship between miRNA in glioma. Methods: Cell proliferation, cell cycle, cell apoptosis and cell migration were analyzed by CCK-8 cell viability, flow cytometry, wound scratch healing, transwell and Western blotting assays, respectively, in vitro. The regulation relationships between TSN and miR-608 or between miR-608 and Notch1 (Notch2) were examined using qRT-PCR, dual-luciferase and Western blotting assays. The functional effects of TSN through regulating miR-608 and Notch1 (Notch2) were further examined using a xenograft tumor mouse model in vivo. Results: After TSN concentration was increased from 50 nM, 100 nM to 150 nM, cell proliferation and cell cycle were gradually reduced, and the cell apoptosis rate was increased in U-138MG or U-251MG cells. Wound-healing and transwell assays results showed that cell migration was significantly inhibited in TSN treatment cells (TSN treatment, 50 nM) compared to control cells. Mechanistic studies revealed that TSN up-regulated the expression of microRNA-608 (miR-608), while down-regulated the expression of miR-608's target, Notch1 and Notch2. Over-expression of Notch1 and Notch2 partly attenuated TSN-induced tumor suppressive function. Moreover, in vivo experiments revealed that TSN treatment led to a significant inhibition of tumor growth, suggesting that it might be a promising drug for the treatment of glioma. Conclusion: In the present study, a novel established functional manner of TSN/miR-608/ Notch1 (Notch2) axis was systematically indicated, which might provide prospective intervention ways for glioma therapy.

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Section: Introductionmentioning

confidence: 99%

<p>Toosendanin Suppresses Glioma Progression Property and Induces Apoptosis by Regulating miR-608/Notch Axis</p>

Wang

Hou

et al. 2020

CMAR

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“…MicroRNA-608 is reported to inhibit cell proliferation in several types of cancers, such as human hepatocellular carcinoma [19], bladder cancer [20], colon cancer [21], and chordoma [22]. Furthermore, it was also demonstrated that microRNA-608 could inhibit the migration and invasion of glioma stem cells [23] and even act as a prognostic marker in hepatocellular carcinoma [24].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of microRNA-608 on lung cancer cell proliferation, migration, and invasion by targeting BRD4 through the JAK2/STAT3 pathway

Sun

Wang

et al. 2019

Bosn J of Basic Med Sci

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BJBMS MOLECULAR BIOLOGY Bosn J Basic Med Sci. 2020;20(3):347-356 347 www.bjbms.org living in developing countries. Therefore, the identification of the mechanisms of lung cancer development is a matter of urgency. MicroRNAs (miRNAs) are small non-coding RNA molecules, containing about 22 nucleotides [5]. These RNAs function in RNA silencing and post-transcriptional regulation of gene expression. Based on the evidence, microRNAs are involved in many cellular processes, such as cell proliferation [6], apoptosis [7], migration [8], invasion [9], epithelial-mesenchymal transition [10], and differentiation [11]. Moreover, the dysregulation of microRNAs also contributes to the development and metastasis of many cancers, such as lung [12], breast [13], gastric [14], ovarian [15], and liver cancers [16].Recent data are indicative of the significantly lower expression of microRNA-608 in lung cancer tissues than in the adjacent normal tissues [17]. Furthermore, another report also revealed that the upregulation of microRNA-608 could increase cell death in A549 and SK-LU1 cells [18]. The results of the aforementioned studies are indicative of the involvement of microRNA-608 in the progression of lung cancer. However, the relationship between microRNA-608 and lung cancer and the molecular mechanism remain to be revealed. ABSTRACTLung cancer is the leading cause of cancer-related mortality around the world. This malignancy has a 5-year survival rate of 21%, because most of the patients are diagnosed in the middle or late stage of the disease when local metastasis and tumor invasion have already progressed. Therefore, the investigation of the pathogenesis of lung cancer is an issue of crucial importance. MicroRNAs (miRNAs) seem to be involved in the evolution and development of lung cancer. MicroRNA-608 is likely to be downregulated in lung cancer tissues. Regarding this, the current study involved the determination of the fundamental mechanism of microRNA-608 in the development of lung cancer. Based on the results of quantitative reverse transcription polymerase chain reaction (RT-qPCR), the expression level of microRNA-608 was downregulated in 40 lung cancer tissues, compared to that in the adjacent normal tissues. The results of dual-luciferase reporter assay revealed that bromodomain-containing protein 4 (BRD4) was the direct target of microRNA-608. Accordingly, the lung cancer tissues had an elevated expression level of BRD4, in contrast to the adjacent normal tissues. The results of Cell Counting Kit 8 assay demonstrated that the high expression of microRNA-608 notably restrained lung cancer cell proliferation. The scratch wound and transwell assays showed that the upregulation of microRNA-608 suppressed the migration and invasion of lung cancer cells. Finally, the western blot assay showed that in the microRNA-608 mimics group, the expression levels of BRD4, p-JAK2, p-STATA3, CD44, and MMP9 were significantly decreased, compared with those in the negative control miRNA mimics group. Our results indicate that high expres...

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“…Higher BRD4 expression was significantly related to poor prognosis in HCC patients, and BRD4 intensity in cancer tissues was an independent prognostic factor for OS [ 23 ]. Mechanistically, over-expression of miR-608 could prevent the proliferation ability of HepG2 cells and HCC growth in mouse xenograft model by down-regulating BRD4 [ 42 ]. Moreover, Wang et al showed that BRD4 promoted HCC cell migration and invasion through inducing matrix metalloproteinase (MMP)-2 and MMP-9, mediated by the Sonic hedgehog signaling pathway [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

BRD4/8/9 are prognostic biomarkers and associated with immune infiltrates in hepatocellular carcinoma

Chen

Ouyang

Chen

et al. 2020

Aging

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Bromodomain (BRD)-containing proteins are a class of epigenetic readers with unique recognition for N-acetyl-lysine in histones and functions of gene transcription and chromatin modification, known to be critical in various cancers. However, little is known about the roles of distinct BRD-containing protein genes in hepatocellular carcinoma (HCC). Most recently, we investigated the transcriptional and survival data of BRD1, BRD2, BRD3, BRD4, BRD7, BRD8, BRD9 in HCC patients through ONCOMINE, UALCAN, Human Protein Atlas, GEPIA, cBioPortal, STRING, TIMER databases. BRD1/2/3/4/7/8/9 were over-expressed in HCC and were significantly associated with clinical cancer stages and pathological tumor grades. High mRNA expressions of BRD4/8/9 were promising candidate biomarkers in HCC patients. The rate of sequence alternations in BRD1/2/3/4/7/8/9 was relatively high (52%) in HCC patients, and the genetic alternations were correlated with shorter overall survival and disease-free survival in HCC patients. Additionally, the mRNA expression levels of individual BRD genes were significantly positively associated with the immune infiltrating levels of B cells, CD8 + T cells, CD4 + T cells, macrophages, neutrophils, and dendritic cells. And the associations between BRD1/2/3/4/7/8/9 and diverse immune marker sets showed a significance. Overall, these results indicated that BRD4/8/9 could be potential prognostic markers and druggable epigenetic targets in HCC patients.

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microRNA-608 inhibits human hepatocellular carcinoma cell proliferation via targeting the BET family protein BRD4

Cited by 19 publications

References 28 publications

<p>Toosendanin Suppresses Glioma Progression Property and Induces Apoptosis by Regulating miR-608/Notch Axis</p>

<p>Toosendanin Suppresses Glioma Progression Property and Induces Apoptosis by Regulating miR-608/Notch Axis</p>

Inhibitory effect of microRNA-608 on lung cancer cell proliferation, migration, and invasion by targeting BRD4 through the JAK2/STAT3 pathway

BRD4/8/9 are prognostic biomarkers and associated with immune infiltrates in hepatocellular carcinoma

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