Selective killing of lung cancer cells by miRNA-506 molecule through inhibiting NF-κB p65 to evoke reactive oxygen species generation and p53 activation

Yin, Mianmian; Ren, Xiangxia; Zhang, X; Luo, Yongde; Wang, G; Huang, Kai; Feng, Shipeng; Bao, Xuanwen; He, Xiaoqi; Liang, Peizhou; Wang, Z; Tang, Hua; He, Jianxing; Zhang, B

doi:10.1038/onc.2013.597

Cited by 93 publications

(65 citation statements)

References 59 publications

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“…Upregulation of miR-506 occurs in 83% lung cancer, however, miR-506 is considered as a tumor suppressor instead of an oncomir. It is known that miR-506 negatively regulates NF-κB p65 expression and thus increases ROS production, which, in turn, activates p53 to kill cancer cells through increased apoptosis (76). …”

Section: Micrornas Regulate Ros Productionmentioning

confidence: 99%

Interplay Between Reactive Oxygen Species and MicroRNAs in Cancer

2016

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Since both reactive oxygen species (ROS) production and microRNAs expression signature have been associated with tumor development, progression, metastasis and therapeutic response, it is important to understand the crosstalk between ROS and microRNAs. Indeed, growing evidence suggests a reciprocal connection between ROS signaling and microRNAs pathway, resulting in diverse biological effects in cancer cells. In this mini review, we discussed the ROS-responsive microRNAs that have implications in cancer and the possible mechanisms in which ROS regulate microRNAs. We also highlighted the microRNAs which are able to modify cellular ROS homeostasis during tumorigenesis, their biological targets and subsequent functions. As the use of antioxidants is limited due to the diverse or even opposing roles of ROS signaling in cancer, the discovery of ROS-responsive microRNAs provides a potential new strategy to specifically overcome ROS-mediated tumor progression or benefit from ROS-induced apoptosis.

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Section: Micrornas Regulate Ros Productionmentioning

confidence: 99%

Interplay Between Reactive Oxygen Species and MicroRNAs in Cancer

2016

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“…Recently, it has been reported that miR-506 inhibits epithelial mesenchymal transition (EMT) in ovarian cancer and breast cancer [10,11] . In addition, miR-506 can significantly restrain the proliferation of lung cancer cells [12] . All these reports suggest that miR-506 is a novel microRNA that is important in the development of cancer.…”

Section: Introductionmentioning

confidence: 99%

MiR-506 suppresses proliferation of hepatoma cells through targeting YAP mRNA 3′UTR

et al. 2014

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Aim: MiR-506 is a miRNA involved in carcinogenesis of several kinds of cancer. In this study, we explored whether miR-506 played a critical role in hepatocellular carcinoma (HCC). Methods: Twenty HCC and adjacent normal liver tissue samples were collected. Human hepatoma cell lines HepG2 and H7402 were used for in vitro studies. The expression of miR-506 and transcriptional co-activator YAP was examined using qRT-PCR. Western blot analysis was used to measure the expression of YAP and its target genes. Luciferase reporter gene assay was used to identify YAP as a target gene of miR-506. MTT and EdU assays were carried out for functional analysis. Results: The expression of miR-506 was significantly lower in HCC than in adjacent normal liver tissues. Bioinformatics analysis revealed that YAP mRNA might be one of the targets of miR-506, and miR-506 in HCC tissues was found to be negatively correlated with YAP (r=-0.605). In both HepG2 and H7402 cells, miR-506 dose-dependently down-regulated YAP and its target genes c-Myc and the connective tissue growth factor (CTGF). Luciferase reporter gene assays demonstrated that miR-506 targeted the wild type 3′UTR of YAP mRNA, but not a 3′UTR with a mutant seed site. Furthermore, miR-506 significantly inhibited the proliferation of HepG2 and H7402 cells, while anti-miR-506 enhanced the cell proliferation, which was blocked by YAP siRNA. Conclusion: MiR-506 suppresses the proliferation of hepatoma cells by targeting YAP mRNA.

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“…In the present study, it was demonstrated that miR-506 functions as a tumor suppressor in neuroblastoma by directly targeting ROCK1. Previous studies have reported that the expression of miR-506 is reduced in numerous types of cancer, including epithelial ovarian cancer (15)(16)(17)(18), hepatocellular carcinoma (19), cervical cancer (20), lung cancer (21), breast cancer (22) and colon cancer (23), and is involved in cancer progression, notably cell proliferation, metastasis and apoptosis. In the current study, it was observed that miR-506 was decreased in neuroblastoma tissues and cell lines when compared to normal tissues, supporting the notion that miR-506 functions as a potential tumor suppressor.…”

Section: Discussionmentioning

confidence: 99%

miR-506 suppresses neuroblastoma metastasis by targeting ROCK1

Cao

et al. 2016

Oncology Letters

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Abstract. Neuroblastoma is a complex form of cancer with highly heterogeneous clinical behavior that arises during childhood from precursor cells of the sympathetic nervous system. In patients with neuroblastoma, mortality often occurs as a result of metastasis. The disease predominantly spreads to bone marrow, with a survival rate of ~40%. The current study demonstrates that microRNA (miR)-506 directly targets and downregulates Rho-associated, coiled-coil containing protein kinase 1 (ROCK1) in transforming growth factor (TGF)-β non-canonical pathways. It may be concluded that ROCK1 contributes to the invasion and migration of neuroblastoma cells by directly downregulating miR-506; thus, leading to the upregulation of ROCK1, which promotes cell invasion and migration. The present results provide a novel understanding of how miR-506 directly regulates TGF-β non-canonical

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Selective killing of lung cancer cells by miRNA-506 molecule through inhibiting NF-κB p65 to evoke reactive oxygen species generation and p53 activation

Cited by 93 publications

References 59 publications

Interplay Between Reactive Oxygen Species and MicroRNAs in Cancer

Interplay Between Reactive Oxygen Species and MicroRNAs in Cancer

MiR-506 suppresses proliferation of hepatoma cells through targeting YAP mRNA 3′UTR

miR-506 suppresses neuroblastoma metastasis by targeting ROCK1

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