Abstract
Hepatoblastoma (HB) is the most common pediatric liver tumor. The significant tumor heterogeneity of HB leads to varied prognoses among children with the disease. Recent studies have suggested that long non-coding RNAs (lncRNAs) can serve as novel therapies for HB treatment. Thus, in this study, we aimed to reveal the function and mechanism of the lncRNA Linc00205 in HB. Our results exhibited that, in both HB tissues and cell lines, levels of Linc00205 were significantly increased. In addition, knockdown of Linc00205 led to suppression of HB development. Moreover, we identified that Linc00205 was able to directly bind to miR-154-3p, thus isolating miR-154-3p from its target Rho-associated coiled-coil Kinase 1 (ROCK1). Further cellular behavioral experiments elucidated that the miR-154-3p inhibitor and ROCK1 overexpression were able to reverse the effect of downregulated Linc00205 on proliferation, migration, invasion, and apoptosis of HB cells by rescue assays via mitogen-activated protein kinase (MAPK) signaling. Our results demonstrated that Linc00205 enhanced HB progression by regulating ROCK1 expression via sponging miR-154-3p through MAPK signaling, which suggests a novel potential therapeutic target for HB.
Highlights
Hepatoblastoma (HB) is the most common primary malignant tumor of the liver among children, as it accounts for over 1% of pediatric malignancies
We performed Quantitative real-time PCR (qRT-PCR) assays in order to determine the expression of Linc00205 in HB tissues and paracancerous normal tissues collected from 60 patients
This study shows that Linc00205 sponges miR-154-3p in order to promote proliferation and metastasis of HB cells by upregulating Rho-associated coiled-coil Kinase 1 (ROCK1)
Summary
Hepatoblastoma (HB) is the most common primary malignant tumor of the liver among children, as it accounts for over 1% of pediatric malignancies. There has been an increase in the incidence of HB, which is thought to be related to a higher number of premature births. HB presents as a solid focal tumor that reproduces the liver in an embryologic development state [2]. The primary curative treatment for HB is surgical excision, and chemotherapy is essential in order to shrink an unresectable tumor to becoming resectable, and decreasing surgery-related morbidity [3]. Children that are within the low-risk category can have an 80% 5-year survival rate after treatment. For children that are high risk or after a relapse, the survival rate decreases to 30-40% [4]. There is a significant need to achieve a more detailed understanding of HB in order to develop more effective therapies to improve patient outcomes
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