MicroRNA-501 promotes HBV replication by targeting HBXIP

Jin, Jianhua; Tang, Shanhong; Lin, Xia; Du, Rui; Xie, Hui; Song, Jiugang; Fan, Rui; Bi, Qian; Chen, Zheng; Yang, Guitao; Liu, Jie; Shi, Yongquan; Fan, Daiming

doi:10.1016/j.bbrc.2012.12.071

Cited by 80 publications

(55 citation statements)

References 17 publications

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“…miR221/222 acts on many key tumor suppressors, including Bmf (29) (35). Among the HBV-related miRNAs, miR1 and miR501-5p can promote HBV replication, thereby promoting the occurrence and progression of HCC (36)(37)(38). In contrast, the decrease of miR122 expression may reduce the antiviral ability of the body and mediate the pathogenesis of primary HCC (39).…”

Section: Discussionmentioning

confidence: 99%

“…These miRNAs execute different biologic functions through acting on different target genes and different signal transduction pathways during the occurrence and development of HCC. These miRNAs can be categorized according to their functions as follows: miR21, miR221/222, miR224, miR17-5p/20a, miR10b, miR106b, miR151-5p, miR155, miR181a/181b, and miR184 can promote the proliferation, invasion, and metastasis of HCC cells (12)(13)(14)(15)(16)(17); miR221/222, miR224, miR10b, and miR155 can inhibit HCC cell apoptosis (13,18,19,21); and miR21, miR221/222, miR143, miR1, and miR501-5p can promote the replication of HBV, induce carcinogenesis, and enhance cancer cell proliferation (36)(37)(38).…”

Section: Discussionmentioning

confidence: 99%

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An Artificially Designed Interfering lncRNA Expressed by Oncolytic Adenovirus Competitively Consumes OncomiRs to Exert Antitumor Efficacy in Hepatocellular Carcinoma

Sun

et al. 2016

Molecular Cancer Therapeutics

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Endogenous miRNAs, especially oncogenic miRNAs (OncomiR), have been molecular targets for cancer therapy. We generated an artificially designed interfering long noncoding RNA (lncRNAi), which contains the sequences that can complementarily bind to multiple OncomiRs and is expressed by cancer-selectively replicating adenovirus. The adenovirus-expressed lncRNAi with high levels in hepatocellular carcinoma (HCC) cells competes with OncomiR target genes to bind to and consume OncomiRs, thereby achieving the targeted anti-HCC efficacy. With the targeting replication of adenovirus in HCC cells, lncRNAi was highly expressed and resulted in decreased abilities of proliferation, migration, and invasion, induced cell-cycle changes and apoptosis, and markedly changed the cellular mRNA and miRNA expression profiles in HCC cells. The optimal antitumor effect was also demonstrated on HCC cell line xenograft models and HCC patient-derived xenograft (PDX) tumor models in nude mice. This strategy has established a technology platform with a reliable therapeutic effect for HCC therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

An Artificially Designed Interfering lncRNA Expressed by Oncolytic Adenovirus Competitively Consumes OncomiRs to Exert Antitumor Efficacy in Hepatocellular Carcinoma

Sun

et al. 2016

Molecular Cancer Therapeutics

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“…For miRNAs promoting HBV replication, it appears that they share a common pattern of targeting a negative cellular regulator of HBV activity. For example, miR-501 targets HBXIP (44), and miR-372/373 targets NFI/B (45). MiR-15b acts in a similar fashion.…”

Section: Discussionmentioning

confidence: 99%

Modulation of HBV replication by microRNA-15b through targeting hepatocyte nuclear factor 1α

Dai

Zhang

et al. 2014

Nucleic Acids Research

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Hepatitis B virus (HBV) infection remains a major health problem worldwide. The role played by microRNAs (miRNAs) in HBV replication and pathogenesis is being increasingly recognized. In this study, we found that miR-15b, an important miRNA during HBV infection and hepatocellular carcinoma development, directly binds hepatocyte nuclear factor 1α (HNF1α) mRNA, a negative regulator of HBV Enhancer I, to attenuate HNF1α expression, resulting in transactivation of HBV Enhancer I, in turn causing the enhancement of HBV replication and expression of HBV antigens, including HBx protein, finally leading to the down-regulated expression of miR-15b in both cell lines and mice in a long cascade of events. Our research showed that miR-15b promotes HBV replication by augmenting HBV Enhancer I activity via direct targeting HNF1α, while HBV replication and antigens expression, particularly the HBx protein, then repress the expression of miR-15b. The reciprocal regulation between miR-15b and HBV controls the level of HBV replication and might play a role in persistent HBV infection. This work adds to the body of knowledge concerning the complex interactions between HBV and host miRNAs.

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“…MiR-122, a special miRNA of liver had been found to downregulate after HBV infection in several studies [13]. In addition, miRNA, including miR-1 [14], miR-181a [15], miR-372 [16], miR-501 [17], was reported to upregulate after HBV infection. Moreover, some miRNAs have been identified to vary according to the development level of disease.…”

Section: Discussionmentioning

confidence: 99%