microRNA expression alteration after arsenic trioxide treatment in HepG‐2 cells

Meng, Xianmin; Zheng, Tongsen; Chen, Xi; Wang, Jiabei; Zhang, Weihui; Pan, Shangha; Jiang, Hongchi; Liu, Lianxin

doi:10.1111/j.1440-1746.2010.06317.x

Cited by 53 publications

(34 citation statements)

References 31 publications

(54 reference statements)

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“…Previous evidence showed that ROS generated by H 2 O 2 (Takagi et al, 2010), hemin (Lal et al, 2009b) or arsenic trioxide (Meng et al, 2011) increased the miR-24 level in human cell lines.…”

Section: Discussionmentioning

confidence: 96%

Aryl hydrocarbon receptor nuclear translocator in human liver is regulated by miR-24

Oda

Nakajima

Mohri

et al. 2012

Toxicology and Applied Pharmacology

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Aryl hydrocarbon receptor nuclear translocator (ARNT) forms a heterodimer with aryl hydrocarbon receptor or hypoxia inducible factor 1α to mediate biological responses to xenobiotic exposure and hypoxia. Although the regulation mechanism of the ARNT expression is largely unknown, earlier studies reported that the human ARNT protein level was decreased by hydrogen peroxide or reactive oxygen species. These stimuli increase the miR-24 level in various human cell lines. In silico analysis predicts that some microRNAs miR-24 would be one of the factors underlying the mechanisms by which ARNT protein is decreased by reactive oxygen species.

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Section: Discussionmentioning

confidence: 96%

Aryl hydrocarbon receptor nuclear translocator in human liver is regulated by miR-24

Oda

Nakajima

Mohri

et al. 2012

Toxicology and Applied Pharmacology

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“…A low level of miR-29 caused loss of inhibition of cyclin E expression, resulting in esophageal carcinoma cell cycle activation (51). Several studies have demonstrated that high expression of miR-29 induces hepatocellular carcinoma cell apoptosis, while downregulation of miR-29 increases HCC tumorigenicity and metastasis (52,53). Mott et al (54) found a high level of miR-29 in normal cholangiocytes by northern blot analysis.…”

Section: Expression Of Mirna-29 In Cancersmentioning

confidence: 98%

Diverse roles of miR-29 in cancer (Review)

et al. 2014

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microRNAs (miRNAs) are non-coding RNAs which have the capacity to regulate gene expression at the post-transcriptional level, and have emerging as key factors involved in cancer at all stages ranging from initiation to metastasis. In the present review, we summmarize the diverse roles of the microRNA-29 (miR-29) family in cancer. First, we present a concise introduction to the miR-29 family and the expression profile of miR-29 in various cancer types. We next highlight the upstream regulatory pathway of miR-29 and describe the relationship between miR-29 and cancer in detail. As a tumor suppressor, miR-29 restrains cancer progression by promoting tumor cell apoptosis, by suppressing DNA methylation of tumor-suppressor genes, by reducing proliferation of tumors and by increasing chemosensitivity. However, as a tumor promoter, miR-29 mediates epithelial-mesenchymal transition (EMT) and promotes metastasis in breast cancer and colon cancer. Finally, we suggest that miR-29 represents a novel diagnostic and prognostic biomarker or a therapeutic target for cancer. Our review highlights the diverse relationship between miR-29 and cancer (particularly digestive system neoplasms). Further research of miR-29 in cancer is warranted.

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“…miR-190 overexpression alone sufficient for acquisition of malignant characteristics in BEAS-2B.Beezold et al, 2011 [77] In vitro exposure to ATO (human hepatocellular carcinoma cell line)4 μM ATO (As 2 O 3 ) for 24 hHuman hepatocellular carcinoma cell line Hep-G2Total RNA analyzed for levels of 677 human miRNAs using a miRNA PCR array. Levels of selected miRNAs analyzed using real-time qPCR.Identified miR-29a as a likely critical mediator of ATO-mediated apoptosis and inhibition of cell growth.Meng et al, 2011 [73] In vitro exposure to arsenite (immortalized human bronchial epithelial cell line)2.5 μM arsenite (NaAsO 2 ) for 16 weeks, resulting in malignant transformationImmortalizedhuman bronchialepithelial cell line p53 low HBEC, which contains stable shRNAknockdown of TP53Total RNA analyzed for levels of 856 human miRNAs using a miRNA PCR array. Levels of selected miRNAs also analyzed using real-time qPCR.Malignant transformation associated with reduction of miR-200 family members; downregulation of miR-200b shown to be essential for malignant transformation.Wang et al, 2011 [76] In vivo exposure to arsenite (chick embryos); in vitro exposure to arsenite (human umbilical cord vein cell line)100 nM arsenite (NaAsO 2 ) injected in yolk sac of chick embryos at HH stages 6, 9, and 12; embryos harvested at HH stage 18.…”

Section: Arsenic and Micrornas (Mirnas)mentioning

confidence: 99%

“…Some of these studies have focused on miRNAs as mediators of the apoptotic effects of arsenic trioxide (ATO) [72, 73], a chemotherapeutic agent used in the treatment of relapsed or refractory acute promyelocytic leukemia [74]. Other studies have indicated miRNAs may play roles in the diverse toxic effects of iAs.…”

Section: Arsenic and Micrornas (Mirnas)mentioning

confidence: 99%

Arsenic-Associated Changes to the Epigenome: What Are the Functional Consequences?

Bailey

Fry

2014

Curr Envir Health Rpt

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Inorganic arsenic (iAs) poses a major threat to worldwide human health, and yet the molecular mechanisms underlying the toxic effects associated with iAs exposure are not well understood. There is increasing experimental evidence indicating that epigenetic modifications may play a major role in the development of diseases associated with exposure to environmental toxicants. Research in the field has firmly established that iAs exposure is associated with epigenetic alterations including changes in DNA methylation, miRNA abundance, and post-translational histone modifications. Here, we summarize recent studies that have expanded the current knowledge of these relationships. These studies have pinpointed specific regions of the genome and genes that are targets of arsenical-induced epigenetic changes, including those associated with in utero iAs exposure. The recent literature indicates that iAs biotransformation likely plays an important role in the relationship between iAs exposure and the epigenome, in addition to the sex and genetic background of individuals. The research also shows that relatively low to moderate exposure to iAs is associated with epigenetic effects. However, while it is well established that arsenicals can alter components of the epigenome, in many cases, the biological significance of these alterations remains unknown. The manner by which these and future studies may help inform the role of epigenetic modifications in the development of iAs-associated disease is evaluated and the need for functional validation emphasized.

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microRNA expression alteration after arsenic trioxide treatment in HepG‐2 cells

Cited by 53 publications

References 31 publications

Aryl hydrocarbon receptor nuclear translocator in human liver is regulated by miR-24

Aryl hydrocarbon receptor nuclear translocator in human liver is regulated by miR-24

Diverse roles of miR-29 in cancer (Review)

Arsenic-Associated Changes to the Epigenome: What Are the Functional Consequences?

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