Regulation of the oncogenic function of distal-less 4 by microRNA-122 in hepatocellular carcinoma

Xie, Xuhua; Xu, Xiaopei; Sun, Cuiyun; Yu, Zujiang

doi:10.3892/mmr.2015.3554

Cited by 10 publications

(7 citation statements)

References 20 publications

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“…However, our investigation did not find the association between DLX4 methylation and BP1 expression in CML patients, which indicated that other mechanism might also be involved in the regulation of BP1 expression. Xie et al demonstrated that down-regulation of DLX4 in hepatocellular carcinoma cell lines was regulated by microRNA-122 through binding to its 3 0 untranslated region [31]. Further studies are needed to determine the other potential mechanism in the regulation of DLX4 expression.…”

Section: Discussionmentioning

confidence: 97%

Epigenetic inactivation of DLX4 is associated with disease progression in chronic myeloid leukemia

Zhou

Wang

Zhang

et al. 2015

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 97%

Epigenetic inactivation of DLX4 is associated with disease progression in chronic myeloid leukemia

Zhou

Wang

Zhang

et al. 2015

Biochemical and Biophysical Research Communications

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“…Accumulating evidence has demonstrated that numerous miRNAs present ectopic expression in HCC patient serum and plasma as well as in HCC cells and tissues; thereby, miRNAs may be useful as novel clinical markers for the early diagnosis, therapeutic monitoring and prognostic prediction of HCC [ 13 ]. For example, miR-122, which is highly abundant in liver, was significantly down-regulated in a large number of HCC patients, ultimately suppressing tumor invasion, proliferation and metastasis in HCC by directly binding to the 3′-UTR of the Distal-less 4 (DLX4) gene [ 14 ]; miR-21, which is markedly up-regulated in HCC, could promote tumor invasion and metastasis and accelerate tumor growth by targeting phosphatase and tensin homolog (PTEN) and programmed cell death 4 (PDCD4) [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

miR-155-5p modulates malignant behaviors of hepatocellular carcinoma by directly targeting CTHRC1 and indirectly regulating GSK-3β-involved Wnt/β-catenin signaling

et al. 2017

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BackgroundHepatocellular carcinoma (HCC) remains one of the most lethal cancers. MicroRNA-155 (miR-155) and collagen triple helix repeat containing 1 (CTHRC1) were found to be involved in hepatocarcinogenesis, but their detailed functions in HCC are unclear. Here, we aimed to investigate the underlying role of miR-155-5p and CTHRC1 in HCC.MethodsmiR-155-5p and CTHRC1 expression levels were detected by qRT-PCR, IHC and WB in HCC patients and cell lines. Dual-luciferase assay, qRT-PCR and WB were used to validate the target interaction between miR-155-5p and CTHRC1. Biological behaviors, including apoptosis, cell cycle progression, and cell proliferation, invasion and migration, were measured by flow cytometry, CCK-8 assay and Transwell tests. A xenograft model was established to examine the effects of miR-155-5p and CTHRC1 on tumor formation. WB was finally utilized to identify the role of GSK-3β-involved Wnt/β-catenin signaling in HCC growth and metastasis.ResultsOur results showed that miR-155-5p and CTHRC1 were down-regulated and up-regulated, respectively, in HCC patients and cell lines. Dual-luciferase assay verified that CTHRC1 was the direct target of miR-155-5p. Moreover, elevated miR-155-5p expression promoted apoptosis but suppressed cell cycle progression and cell proliferation, invasion and migration in vitro and facilitated tumor formation in vivo; elevated CTHRC1 expression abolished these biological effects. Additionally, miR-155-5p overexpression increased metastasis- and anti-apoptosis-related protein expression and decreased pro-apoptosis-related protein expression, while forced CTHRC1 expression conserved the expression of these proteins.ConclusionAltogether, our data suggested that miR-155-5p modulated the malignant behaviors of HCC by targeting CTHRC1 and regulating GSK-3β-involved Wnt/β-catenin signaling; thereby, miR-155-5p and CTHRC1 might be promising therapeutic targets for HCC patients.Electronic supplementary materialThe online version of this article (10.1186/s12935-017-0469-8) contains supplementary material, which is available to authorized users.

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“…Xu Q et al reported that overexpression of miR-122 repressed proliferation but induced apoptosis by targeting pyruvate kinase muscle 2 (PKM2) in HCC 72 . Another report found that miR-122 could downregulate the expression of oncogenic distal-less 4 (DLX4), knockdown the expression of this oncogene would inhibit HCC cells proliferation 73 . Overexpression of miR-137 was reported to reduce HepG2 cells proliferation by targeting EZH2 76 .…”

Section: Mirnas and Proliferation And Apoptosis Of Hccmentioning

confidence: 99%

The Role of MicroRNAs in Hepatocellular Carcinoma

et al. 2018

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Hepatocellular carcinoma (HCC) is one of the most common cancers, leading to the second cancer-related death in the global. Although the treatment of HCC has greatly improved over the past few decades, the survival rate of patients is still quite low. Thus, it is urgent to explore new therapies, especially seek for more accurate biomarkers for early diagnosis, treatment and prognosis in HCC. MicroRNAs (miRNAs), small noncoding RNAs, are pivotal participants and regulators in the development and progression of HCC. Great progress has been made in the studies of miRNAs in HCC. The key regulatory mechanisms of miRNAs include proliferation, apoptosis, invasion, metastasis, epithelial-mesenchymal transition (EMT), angiogenesis, drug resistance and autophagy in HCC. And exosomal miRNAs also play important roles in proliferation, invasion, metastasis, and drug resistance in HCC by regulating gene expression in the target cells. In addition, some miRNAs, including exosomal miRNAs, can be as potential diagnostic and prediction markers in HCC. This review summarizes the latest researches development of miRNAs in HCC in recent years.

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Regulation of the oncogenic function of distal-less 4 by microRNA-122 in hepatocellular carcinoma

Cited by 10 publications

References 20 publications

Epigenetic inactivation of DLX4 is associated with disease progression in chronic myeloid leukemia

Epigenetic inactivation of DLX4 is associated with disease progression in chronic myeloid leukemia

miR-155-5p modulates malignant behaviors of hepatocellular carcinoma by directly targeting CTHRC1 and indirectly regulating GSK-3β-involved Wnt/β-catenin signaling

The Role of MicroRNAs in Hepatocellular Carcinoma

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