Objective: This study is performed to explore the role of transcription factor FOXM1 in promoting the self-renewal and proliferation of liver cancer stem cells (LCSCs) by regulating the expression of acetaldehyde dehydrogenase-2 (ALDH2). Methods: CD133 + CD24 + LCSCs were sorted and identified. A series of experiments were carried out to determine the proliferation, colony formation rate, migration, invasion, and apoptosis of LCSCs after interfering with FOXM1. Proliferation-, epithelial-mesenchymal transition (EMT)-, apoptosis-, and stemness-related factors were then detected by western blot analysis. Tumor xenograft in nude mice was used to figure out the role of FOXM1 in tumorigenesis in vivo by regulating ALDH2 expression. Luciferase activity assay was conducted to determine whether FOXM1 could target ALDH2 promoter region and thereby affecting ALDH2 expression. Results: The sorted CD133 + CD24 + Huh-7 cells had the characteristic of stem cells. FOXM1 was highly expressed in CD133 + CD24 + Huh-7 cells. Silencing FOXM1 inhibited the proliferation and colony formation of LCSCs and decreased the expression of proliferating cell nuclear antigen and Ki-67 protein; inhibited the migration, invasion, and EMT of LCSCs while promoting the apoptosis of LCSCs, as well as promoted the expression of Bax and cleaved-caspase-3, and inhibited the expression of Bcl-2. Silencing FOXM1 inhibited the expression of Nanog, Oct4, and Sox2 in LCSCs by decreasing the expression of ALDH2. in vivo experiment, silencing FOXM1 suppressed tumorigenesis of LCSCs by decreasing the expression of ALDH2.

Objective: has been shown to participate in multiple malignancies, but the role of miR-203 in hepatoblastoma (HB) remains unclear. The aim of our study was to investigate the effects of miR-203 in HB. Methods: A total of 15 pairs of HB tissues and para-tumour normal tissues were collected for the experiments. RT-qPCR and Western blotting were performed to detect the expression of CRNDE, miR-203, and VEGFA at the mRNA and/or protein levels, respectively. A dual luciferase assay verified the target relationship between miR-203 and the 3′UTR of VEGFA as well as miR-203 and CRNDE. In addition, MTT, wound healing, and tube formation assays were performed to assess the effects of miR-203, VEGFA, and CRNDE on cell proliferation, migration, and angiogenesis, respectively. Results: Our data revealed that miR-203 expression was decreased in HB tissues, while long non-coding RNA (lncRNA) CRNDE expression was increased. The dysregulation of miR-203 and CRNDE was closely related to tumour size and stage. Moreover, overexpression of miR-203 inhibited angiogenesis. A dual luciferase assay verified that VEGFA is a direct target of miR-203 and that CRNDE binds to miR-203. Furthermore, our results showed that miR-203 suppressed cell viability, migration, and angiogenesis by regulating VEGFA expression. Additionally, it was confirmed that CRNDE promoted angiogenesis by negatively regulating miR-203 expression. Conclusion: lncRNA CRNDE targets the miR-203/VEGFA axis and promotes angiogenesis in HB. These results provide insight into the underlying mechanisms of HB and indicate that CRNDE and miR-203 might be potential targets for HB therapy.

Liver ischemia-reperfusion injury (IRI) is a major complication of liver trauma, resection, and transplantation. IRI may lead to liver dysfunction and failure, but effective approach to address it is still lacking. To better understand the cellular and molecular mechanisms of liver IRI, functional roles of numerous cell types, including hepatocytes, Kupffer cells, neutrophils, and sinusoidal endothelial cells, have been intensively studied. In contrast, hepatic stellate cells (HSCs), which are well recognized by their essential functions in facilitating liver protection and repair, have gained less attention in their role in IRI. This review provides a comprehensive summary of the effects of HSCs on the injury stage of liver IRI and their associated molecular mechanisms. In addition, we discuss the regulation of liver repair and regeneration after IRI by HSCs. Finally, we highlight unanswered questions and future avenues of research regarding contributions of HSCs to IRI in the liver.

Hepatoblastoma is the most common malignant hepatic tumour type with hypervascularity in early childhood. in recent decades, emerging evidence has proven that long non-coding rnas (lncrnas) serve an important oncogenic role in the pathogenesis of hepatoblastoma. However, the underlying mechanism of lncrna taurine upregulated 1 (TuG1) in the angiogenesis of hepatoblastoma remains unknown. The expression patterns of TuG1 and microrna (mir)-204-5p were detected in hepatoblastoma tissues and cell lines via reverse transcription-quantitative Pcr and were analysed using a Pearson's correlation test. a tube formation assay was performed using human umbilical vein endothelial cells to assess the vasculogenic activity of treated HuH-6 cells. eliSa was used to detect the level of the secretory proangiogenic factor VeGFa in the culture media of HuH-6 cells. a dual luciferase reporter assay was performed to validate the binding relationships of TuG1/mir-204-5p and mir-204-5p/Janus kinase 2 (JaK2). Moreover, western blotting was conducted to measure the protein expression levels of VeGFa, phosphorylated (p)-JaK2, JaK2, p-STaT3 and STaT3. it was identified that TuG1 was upregulated, while mir-204-5p was downregulated in hepatoblastoma tissues and cells. TuG1 knockdown inhibited angiogenesis induced by hepatoblastoma cells. Furthermore, mir-204-5p was identified as a target of TUG1. The results demonstrated that TuG1 attenuated the inhibitory effect of mir-204-5p on the JaK2/STaT3 pathway and promoted angiogenesis in hepatoblastoma cells. in summary, TuG1 was upregulated in hepatoblastoma and suppressed mir-204-5p, thereby activating the downstream signalling pathway of JaK2/STaT3 to facilitate angiogenesis. The present findings will provide novel targets for the treatment of hepatoblastoma.