Arsenic trioxide attenuates the invasion potential of human liver cancer cells through the demethylation-activated microRNA-491

Wang, Xingxing; Jiang, Fei; Mu, Juan; Ye, Xianqing; Si, Lu; Ning, Shilong; Zhong, Li; Li, Yuan

doi:10.1016/j.toxlet.2014.03.016

Cited by 48 publications

(39 citation statements)

References 38 publications

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“…Many human malignancies are associated with dysregulation of miRNAs, and miR-491 functions as an important tumor suppressor in many human malignancies [19,20]. MiR-491 suppresses the proliferation of colorectal cancer cells by promoting cell apoptosis via targeting Bcl-XL [21].…”

Section: Discussionmentioning

confidence: 99%

A Single Nucleotide Polymorphism (rs1056629) in 3'-UTR of MMP-9 is Responsible for a Decreased Risk of Metastatic Osteosarcoma by Compromising its Interaction with microRNA-491-5p

Tian

2016

Cell Physiol Biochem

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Background: This study aimed to explore the roles of microRNA-491-5p (miR-491) and its target MMP9 in the control of metastasis of osteosarcoma (OS) as well as how the rs1056629 polymorphism in the 3' untranslated region (3'UTR) of MMP9 compromises the interaction between miR-491 and MMP9. Methods: We used bioinformatics tools to identify possible binding sites of miR-491 in the 3'UTR of MMP9 and 30 OS tissue samples were collected and divided into two groups based on the rs1056629 genotype (AA, N=20; AC, N=8; and CC N=2). The expression of miR-491 and MMP9 were determined in those samples. Results: We found that the rs1056629 polymorphism potentially compromised the interaction between miRNA and mRNA, which was subsequently confirmed by using the luciferase reporter system. we found that the expression of miR-491 was comparable among the genotype groups, whereas the expression of MMP9 was much higher in the AC/CC groups than in the AA group. Furthermore, 10 OS cell lines (OSA, MG-63, Saos-2, U2OS, SARG, KPD, OHS, HAL, ZK-58, and MHM) were genotyped for the rs1056629 polymorphism, and MG-63 (AA) and OSA (AC) were identified for the scratch test and Transwell assay that followed. In the MG-63 cells, transfection of the miR-491 mimics and MMP9 siRNA similarly and substantially down regulated the expression of MMP9, and miRNA and siRNA clearly suppressed the migratory and invasive ability. In the OSA cells, only MMP9 siRNA notably reduced the expression of MMP9 and decreased the migratory and invasive ability. The introduction of miR-491 mimics left the expression of MMP9 and the migratory and invasive ability intact. Conclusion: We found that the rs1056629 polymorphism interfered with the interaction between MMP9 mRNA and miR-491 and is associated with the metastasis of OS cells.

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Section: Discussionmentioning

confidence: 99%

A Single Nucleotide Polymorphism (rs1056629) in 3'-UTR of MMP-9 is Responsible for a Decreased Risk of Metastatic Osteosarcoma by Compromising its Interaction with microRNA-491-5p

Tian

2016

Cell Physiol Biochem

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“…Since the remarkable therapeutic effect of As 2 O 3 on acute promyelocytic leukemia (APL) was recognized (2), an increasing number of researchers have reported its potential anticancer activity in solid tumors, including hepatocellular carcinoma (3,4), and pancreatic (5), prostate (6) and cervical cancer (7). However, the effect of As 2 O 3 on lung cancer, which is the leading cause of cancer mortality worldwide (8), has been poorly explored.…”

Section: Introductionmentioning

confidence: 99%

Anti-angiogenic effect of arsenic trioxide in lung cancer via inhibition of endothelial cell migration, proliferation and tube formation

et al. 2017

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Abstract. Arsenic trioxide (As 2 O 3 ) exhibits a remarkable effect on leukemia treatment; however, its effect on solid tumors remains poorly explored. The present study demonstrated the inhibitory effect of As 2 O 3 on lung cancer and explored its possible mechanism. It was observed that As 2 O 3 significantly inhibited the growth of lung cancer xenografts and tumor angiogenesis in vivo. The inhibitory effect of As 2 O 3 on cell proliferation in vitro was more remarkable in vascular endothelial cells than in lung cancer cells. It was also observed that As 2 O 3 inhibited the migration of vascular endothelial cells and disrupted vascular tube formation on Matrigel assays. In addition, a series of key signaling factors involved in multiple stages of angiogenesis, including matrix metalloproteinase (MMP)-2, MMP-9, platelet-derived growth factor (PDGF)-BB/PDGF receptor-β, vascular endothelial growth factor (VEGF)-A/VEGF receptor-2, basic fibroblast growth factor (FGF)/FGF receptor-1 and delta like canonical Notch ligand 4/Notch-1, were regulated by As 2 O 3 . These findings suggested that anti-angiogenesis may be an underlying mechanism of As 2 O 3 anticancer activity in lung cancer.

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“…Hepatocellular carcinoma (HCC) is the fifth leading cause of cancer-associated mortality in the USA, with an estimated annual diagnosis rate of 33,190 people and an annual mortality rate of 23,000 cases in 2014 (1). Despite significant advances in the diagnosis and treatment of HCC, its prognosis is poor.…”

Section: Introductionmentioning

confidence: 99%

BRD4 induces cell migration and invasion in HCC cells through MMP-2 and MMP-9 activation mediated by the Sonic hedgehog signaling pathway

Wang

Sui

et al. 2015

Oncology Letters

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Abstract. Hepatocellular carcinoma (HCC) is a highly aggressive form of carcinoma with poor prognosis, and HCC-associated mortality primarily occurs due to migration and invasion of HCC cells. The manipulation of epigenetic proteins, such as BRD4, has recently emerged as an alternative therapeutic strategy. The present study aimed to investigate the novel mechanism of BRD4 involvement in the migration and invasion of HCC cells. Reverse transcription-quantitative polymerase chain reaction was used to assess BRD4 mRNA expression levels in HCC cell lines. This analysis demonstrated that BRD4 was significantly overexpressed in HCC cell lines compared with a human immortalized normal liver cell line. A short hairpin RNA (shRNA) was then used to suppress BRD4 expression in HCC cells, and resulted in impaired HCC cell proliferation, migration and invasion. When the HepG2 HCC cell line was treated with recombinant human sonic hedgehog (SHH) peptide, the migration and invasion capabilities of HepG2 cells that were inhibited by BRD4 silencing were restored. BRD4 induced cell migration and invasion in HepG2 cells through the activation of matrix metalloproteinase (MMP)-2 and MMP-9, mediated by the SHH signaling pathway. Taken together, the results of the present study demonstrated the importance of BRD4 in HCC cell proliferation and metastasis. Thus, BRD4 is a potential novel target for the development of therapeutic approaches against HCC.

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Arsenic trioxide attenuates the invasion potential of human liver cancer cells through the demethylation-activated microRNA-491

Cited by 48 publications

References 38 publications

A Single Nucleotide Polymorphism (rs1056629) in 3'-UTR of MMP-9 is Responsible for a Decreased Risk of Metastatic Osteosarcoma by Compromising its Interaction with microRNA-491-5p

A Single Nucleotide Polymorphism (rs1056629) in 3'-UTR of MMP-9 is Responsible for a Decreased Risk of Metastatic Osteosarcoma by Compromising its Interaction with microRNA-491-5p

Anti-angiogenic effect of arsenic trioxide in lung cancer via inhibition of endothelial cell migration, proliferation and tube formation

BRD4 induces cell migration and invasion in HCC cells through MMP-2 and MMP-9 activation mediated by the Sonic hedgehog signaling pathway

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