Abstract
Hepatoblastoma is the most common hepatic malignancy during childhood. However, little is still known about the molecular mechanisms that govern the development of this disease. This review is focused on the recent advances regarding the study of microRNAs in hepatoblastoma and their substantial contribution to improv our knowledge of the pathogenesis of this disease. We show here that miRNAs represent valuable tools to identify signaling pathways involved in hepatoblastoma progression as well as useful biomarkers and novel molecular targets to develop alternative therapeutic strategies in this disease.
Highlights
Hepatoblastoma (HB) is a pediatric tumor that arises from hepatic progenitors or hepatoblasts.It is the most common malignancy of the liver occurring in the pediatric population, with an annual incidence rate of 1.5 cases per million that represents around 1% of total cancers in childhood [1].its incidence has increased by 2.7% per year over the last decades, probably due to the improved survival of premature infants [2]
Progressive advances in surgical techniques and chemotherapy regimens have resulted in higher survival rates in cases with localized disease, but in that 25% of cases who develop metastases, the prognosis remains very poor [4]
The Wnt/β-catenin, Myc, and Hippo pathways have been reported to be involved in the pathogenesis of HB tumors, little is still known about the molecular basis of this disease
Summary
Hepatoblastoma (HB) is a pediatric tumor that arises from hepatic progenitors or hepatoblasts. MiRNA genes are transcribed by RNA polymerase II The pre-miR is cleaved by Dicer and the mature miR binds to the RNA-induced silencing complex (RISC) and targets a specific mRNA. MiRNAs play a key role in regulating processes like proliferation, differentiation, apoptosis, invasion, angiogenesis, and metastasis via gene expression manipulation [9]. MiRNAs expression is frequently deregulated in many tumors and their specific target genes determine whether they act as tumor suppressors or oncogenes in human cancers [9]. The c-MYC oncoprotein induces the expression of the miR-17-92 cluster [16] and represses the transcription of many miRNAs with tumor suppressor roles, such as the let-7 family [17]. In nasopharyngeal carcinoma cells, the miR-15a/16-1 cluster controls angiogenesis by targeting the angiogenic factors VEGFA and MET [23]
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