The inhibition of microRNA-15a suppresses hepatitis B virus-associated liver cancer cell growth through the Smad/TGF-β pathway

Wang, Yan

doi:10.3892/or.2017.5618

Cited by 10 publications

(10 citation statements)

References 22 publications

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“…To date, modulation of Smad signaling in the context of viral infections are almost exclusively in the context of chronic infections, in particular virally-induced cancers [ 88 – 91 ]. Whether this alteration in chronic infections is a consequence of oncogenesis or virally mediated is not known.…”

Section: Discussionmentioning

confidence: 99%

Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection

et al. 2018

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Rift Valley fever virus (RVFV) infects both ruminants and humans leading to a wide variance of pathologies dependent on host background and age. Utilizing a targeted reverse phase protein array (RPPA) to define changes in signaling cascades after in vitro infection of human cells with virulent and attenuated RVFV strains, we observed high phosphorylation of Smad transcription factors. This evolutionarily conserved family is phosphorylated by and transduces the activation of TGF-β superfamily receptors. Moreover, we observed that phosphorylation of Smad proteins required active RVFV replication and loss of NSs impaired this activation, further corroborating the RPPA results. Gene promoter analysis of transcripts altered after RVFV infection identified 913 genes that contained a Smad-response element. Functional annotation of these potential Smad-regulated genes clustered in axonal guidance, hepatic fibrosis and cell signaling pathways involved in cellular adhesion/migration, calcium influx, and cytoskeletal reorganization. Furthermore, chromatin immunoprecipitation confirmed the presence of a Smad complex on the interleukin 1 receptor type 2 (IL1R2) promoter, which acts as a decoy receptor for IL-1 activation.

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Section: Discussionmentioning

confidence: 99%

Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection

et al. 2018

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“…Between these miRs, miR-15a and miR-210 have been described with protumoral properties. MiR-15a expression has been found to be upregulated in liver cancer tissues associated with hepatitis B. Smad 7, which blocks TGF-β signaling, is a target of miR-15a in these tissues, leading to the suppression of cell growth 92 . MiR-210 has been reported to promote angiogenesis of liver cancers and in high levels is an indicator of HCC poor prognosis.…”

Section: Discussionmentioning

confidence: 99%

Human amniotic membrane conditioned medium inhibits proliferation and modulates related microRNAs expression in hepatocarcinoma cells

Riedel

Pérez-Pérez

Carmona-Fernández

et al. 2019

Sci Rep

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The placental stem cells have called the focus of attention for their therapeutic potential to treat different diseases, including cancer. There is plenty evidence about the antiproliferative, antiangiogenic and proapoptotic properties of the amniotic membrane. Liver cancer is the fifth cause of cancer in the world, with a poor prognosis and survival. Alternative treatments to radio- or chemotherapy have been searched. In this work we aimed to study the antiproliferative properties of the human amniotic membrane conditioned medium (AM-CM) in hepatocarcinoma cells. In addition, we have analyzed the regulation of pro and antiOncomiRs expression involved in hepatocarcinoma physiology. We have determined by 3H-thymidine incorporation assay that AM-CM inhibits DNA synthesis in HepG2 cells after 72 h of treatment. AM-CM pure or diluted at 50% and 25% also diminished HepG2 and HuH-7 cells viability and cell number. Furthermore, AM-CM induced cell cycle arrest in G2/M. When proliferation mechanisms were analyzed we found that AM-CM reduced the expression of both Cyclin D1 mRNA and protein. Nuclear expression of Ki-67 was also reduced. We observed that this CM was able to promote the expression of p53 and p21 mRNA and proteins, leading to cell growth arrest. Moreover, AM-CM induced an increase in nuclear p21 localization, observed by immunofluorescence. As p53 levels were increased, Mdm-2 expression was downregulated. Interestingly, HepG2 and HuH-7 cells treatment with AM-CM during 24 and 72 h produced an upregulation of antiOncomiRs 15a and 210, and a downregulation of proOncomiRs 206 and 145. We provide new evidence about the promising novel applications of human amniotic membrane in liver cancer.

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“…Xie et al [11] proved that serum miRNA-101 level is a candidate biomarker to differentiate HBV-HCC and HBV-cirrhosis. Wang et al [12] demonstrated that the inhibition of miRNA-15a suppresses the proliferation of HBV-infected HepG2 cells [12]. MiRNA-210 is a hypoxia-regulated-miRNA that participates in the tumorigenesis and progression of HCC [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Silencing of microRNA-210 inhibits the progression of liver cancer and hepatitis B virus-associated liver cancer via targeting EGR3

Mei

Song

et al. 2020

BMC Med Genet

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Background: This study was aimed to investigate the regulatory role of microRNA-210 (miRNA-210) on the progression of liver cancer and Hepatitis B virus (HBV)-associated liver cancer. Methods: The expression of miRNA-210 was detected in liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells by qRT-PCR. MiRNA-210 was silenced in HepG2 and HepG2.2.15 cells by the transfection of miRNA-210 inhibitor. The cell viability and apoptosis was detected by MTT assay and Annexin Vfluorescein isothiocyanate/propidium iodide staining, respectively. The protein expression of EGR3 was detected by Western blot. The regulatory relationship between EGR3 and miRNA-210 was predicted by TargetScan and identified by Dual luciferase reporter gene assay.Results: MiRNA-210 was overexpressed in the liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells (P < 0.05). Silencing of miRNA-210 inhibited the viability and promoted the apoptosis of HepG2 and HepG2.2.15 cells (P < 0.05). EGR3 was a target of miRNA-210, which was down-regulated in the liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells (P < 0.05). Silencing of miRNA-210 increased the mRNA and protein expression of EGR3 (P < 0.05). Silencing of EGR3 reversed the antitumor effect of miRNA-210 inhibitor on HepG2 and HepG2.2.15 cells (P < 0.05). Conclusions:Silencing of miRNA-210 inhibits the progression of liver cancer and HBV-associated liver cancer via up-regulating EGR3.

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The inhibition of microRNA-15a suppresses hepatitis B virus-associated liver cancer cell growth through the Smad/TGF-β pathway

Cited by 10 publications

References 22 publications

Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection

Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection

Human amniotic membrane conditioned medium inhibits proliferation and modulates related microRNAs expression in hepatocarcinoma cells

Silencing of microRNA-210 inhibits the progression of liver cancer and hepatitis B virus-associated liver cancer via targeting EGR3

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