Human hepatocellular carcinoma cell-specific miRNAs reveal the differential expression of miR-24 and miR-27a in cirrhotic/non-cirrhotic HCC

Salvi, Alessandro; Abeni, Edoardo; Portolani, Nazario; Barlati, Sergio; Petro, Giuseppina De

doi:10.3892/ijo.2012.1716

Cited by 47 publications

(38 citation statements)

References 37 publications

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“…The expression of miR-24 was significantly reduced in HCC with cirrhosis compared to adjacent cirrhotic tissue, suggesting an influence on hepatocyte carcinogenic transformation of cirrhotic tissues. [24] Significant down-regulation of miR-130a was observed in over 75% (78/102) of HCC tumor tissues. [25] The same repression pattern of miR-130a was also found in HCV-infected human HCC cells [26] and rat liver tissue after treatment with AFB 1 , a strong hepatocarcinogen.…”

Section: Discussionmentioning

confidence: 99%

Identifying microRNA panels specifically associated with hepatocellular carcinoma and its different etiologies

Shen

Siegel

Remotti

et al. 2016

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Aim Deregulation of microRNAs (miRNAs) expression has been identified in hepatocellular carcinoma (HCC), but few results are consistent. The objective of this study is to investigate “HCC tumor type specific” and “tumor common” miRNA panels Methods The authors integrate and analyze clinical, etiologic and miRNA profiles data from 9 types of solid tumors in The Cancer Genome Atlas (TCGA) and HCC data from Columbia University Medical Center (CUMC). Results Levels of 33 miRNAs were significant different between HCC tumor and paired non-tumor tissues (over 2-fold changes) after Bonferroni correction for multiple comparisons, and most (28 miRNAs) were down-regulated in HCC tumors. Using this panel, the authors well classified HCC tumor tissues with 4 misclassifications among 48 paired tissues. Validating this panel in an additional 302 HCC tumor tissues, the authors almost perfectly distinguished tumor from non-tumor tissues with only two misclassifications (99% of HCC tissues correctly classified). Evaluating miRNA profiles in 32 independent HCC paired tissues from CUMC, the authors observed 40 miRNAs significantly deregulated in HCC with over 2-fold changes; 14 overlapped with those identified in TCGA. Subgroup analyses by HCC etiology found that 4 upregulated and 8 downregulated miRNAs were significantly associated with alcohol-related HCC. There were 7 and 4 miRNAs significantly associated with hepatitis B virus- and hepatitis C virus-related HCC, respectively. Data for the first time revealed that miR-24-1, miR-130a and miR-505 were significantly down-regulated only in HCC tumors; miR-142 and miR-455 were significantly down-regulated in HCC, but up-regulated in 5 other solid tumors; suggesting their HCC “tumor type specific” characteristics. A panel of 8 miRNAs was significant in at least 5 tumor types, including HCC, and was identified as “tumor common” marker. Conclusion The authors concluded that aberrant miRNA panels have HCC “tumor type specificity” and may be affected by etiologic factors.

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Section: Discussionmentioning

confidence: 99%

Identifying microRNA panels specifically associated with hepatocellular carcinoma and its different etiologies

Shen

Siegel

Remotti

et al. 2016

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“…However, deregulated miRNAs and their detailed molecular roles in tumorigenesis are still not well understood. Recently, miR-24 has been shown to be aberrantly altered in some cancers, including HCC [10][11][12]. However, the role of miR-24 in carcinogenesis and progression of HCC remains largely elusive.…”

Section: Introductionmentioning

confidence: 98%

miR-24 promotes the proliferation and invasion of HCC cells by targeting SOX7

She

Ming

et al. 2014

Tumor Biol.

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Accumulating evidence shows that microRNAs (miRNAs) are involved in the development and progression of multiple tumors, including hepatocellular carcinoma (HCC). Recent studies have found that miR-24 acts as an oncogene in several tumors; however, the function of miR-24 in HCC remains unclear. In this study, we found that miR-24 was increased in HCC tissues and cell lines. Inhibition of miR-24 by inhibitor significantly suppressed HCC cells proliferation, migration, and invasion. Furthermore, the sex-determining region Y (SRY)-box 7 (SOX7), a putative tumor suppressor, was found to be a target of miR-24 in HCC cells. Forced expression of SOX7 substantially attenuated the oncogenic effects of miR-24. Those results strongly suggest that miR-24 plays important role in HCC development partially by targeting SOX7.

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“…The discovery of miRNAs has increased our understanding of the post-transcriptional regulation of genes and how this contributes to diverse physiological, developmental, and pathophysiological processes, including cancer initiation and progression (Wang et al, 2012). Several studies have linked deregulation of miRNA expressions to HCC carcinogenesis and metastasis in recent years (Budhu et al, 2008, Salvi et al, 2013). Thus, miRNAs may become promising candidates for therapeutic targets.…”

Section: Introductionmentioning

confidence: 99%

The miR-367-3p Increases Sorafenib Chemotherapy Efficacy to Suppress Hepatocellular Carcinoma Metastasis through Altering the Androgen Receptor Signals

Lin

et al. 2016

EBioMedicine

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The androgen receptor (AR) was found to suppress hepatocellular carcinoma (HCC) metastasis at late stages. Due to this discovery, we searched for some AR enhancers to increase the efficacy of Sorafenib chemotherapy, and identified the microRNA (miR)-367-3p, whose expression is positively correlated with AR expression in advanced HCC, as an HCC metastasis suppressor. Combining miR-367-3p with Sorafenib showed better efficacy to suppress HCC cell invasion in vitro and in vivo. Mechanism dissection revealed that miR-367-3p could increase AR expression via directly targeting the 3′UTR of MDM2 to decrease MDM2 protein expression. The resultant increase of AR expression might then promote the expression of FKBP5 and PHLPP, thus dephosphorylating and inactivating AKT and ERK, to suppress the HCC cell invasion. Interestingly, the suppression of pAKT by miR-367-3p could subsequently attenuate the phosphorylation of AR and MDM2, giving rise to additional enhancement of AR protein expression, effectively forming a positive feedback loop. Together, these results suggest that miR-367-3p may function as an AR enhancer to increase Sorafenib chemotherapy efficacy via altering the MDM2/AR/FKBP5/PHLPP/(pAKT and pERK) signals to better suppress HCC metastasis. Successful development of this newly combined chemotherapy in the future may help us to better suppress the HCC metastasis at late stages.

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Human hepatocellular carcinoma cell-specific miRNAs reveal the differential expression of miR-24 and miR-27a in cirrhotic/non-cirrhotic HCC

Cited by 47 publications

References 37 publications

Identifying microRNA panels specifically associated with hepatocellular carcinoma and its different etiologies

Identifying microRNA panels specifically associated with hepatocellular carcinoma and its different etiologies

miR-24 promotes the proliferation and invasion of HCC cells by targeting SOX7

The miR-367-3p Increases Sorafenib Chemotherapy Efficacy to Suppress Hepatocellular Carcinoma Metastasis through Altering the Androgen Receptor Signals

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