The long noncoding RNAs (lncRNAs) have long been clarified to participate in hepatocellular carcinoma (HCC) as a biomarker. We carried out the present study in order to identify HCC-related lncRNAs and elucidate the functional roles in the development and progression of HCC. Our previous study has provided that LINC01225 may be an HCC-related gene. Here, we verified that LINC01225 was upregulated in HCC. Knockdown of LINC01225 resulted in inhibited cell proliferation and invasion with activated apoptosis and cell cycle arrest in vitro. Overexpression of LINC01225 in LINC01225 knockdown cells presented that attenuated cell proliferation and invasion were restored and enhanced. Subcutaneous and tail vein/intraperitoneal injection xenotransplantation model in vivo validated reduced tumor progression and metastasis. Investigation of mechanism found that LINC01225 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR, and subsequently fine tune the EGFR/Ras/Raf-1/MEK/MAPK signaling pathway. Analysis with clinicopathological information suggested a high expression of LINC01225 is positively associated with poor prognosis. We also proved that LINC01225 was stably expressed in serum and can act as a novel biomarker in predicting the diagnosis of HCC. As a conclusion, LINC01225 plays a crucial role in HCC and can act as a biomarker for the diagnosis and prognosis of HCC.

Objective: To determine plasma apolipoprotein M (apoM) levels and other lipid profiles in hepatocellular carcinoma (HCC) patients compared to other chronic liver diseases and normal subjects. Materials and methods: 36 HCC, 68 chronic hepatitis, 29 liver cirrhosis patients and 64 normal controls were subjected in the present study. Serum lipids, lipoproteins, apolipoprotein AI (apoAI) and apoB were determined by the conventional methods. Plasma apoM levels were semi-quantitatively determined by both dot-blotting and western blotting analysis. Results: Serum levels of triglycerides (TG), HDL-cholesterol, apoAI and lipoprotein (a) (Lp(a)) were significantly lower in the HCC patients than in the normal subjects, whereas there were no obvious differences on serum total cholesterol, LDL-cholesterol and apoB between HCC patients and normal subjects. However, plasma apoM levels in HCC patients were significantly increased than those in the normal subjects, but lower than those in the chronic hepatitis and cirrhosis patients. Conclusion: It is concluded that serum TG, apoAI, HDL-C and Lp(a) were significantly decreased in HCC patients than in controls, whereas plasma apoM levels were significantly increased in the HCC patients. Decreased serum TG, apoAI, HDL-C and Lp(a) may reflect the liver damage in HCC patients, whereas the clinical significance of increased plasma apoM levels in relation to HCC is not clear.

Enhanced Myd88 expression has been found in various parenchymal tumors especially in hepatocellular carcinoma with little mechanism of its upregulation known. A lot of long non-coding RNAs are reported to regulate the protein-coding genes which have location association through various mechanisms. In our study we confirmed a new long non-coding RNA Myd88 aberrant upregulated in HCC located upstream of Myd88 and verified a positive regulation relationship between them indicating that Lnc-Myd88 might participate in the enhanced expression of Myd88 in HCC. The gain- and loss-of-function analysis revealed that Lnc-Myd88 could promote the proliferation and metastasis of HCC both in vitro and in vivo. In addition, ChIP assays demonstrated that Lnc-Myd88 might increase Myd88 expression through enhancing H3K27Ac in the promoter of Myd88 gene, thus resulting in the activation of both NF-κB and PI3K/AKT signal pathways. In conclusion, we proposed that Lnc-Myd88 might serve as a novel diagnosis and therapeutic target for HCC.

Pancreatic cancer is a deadly disease, the deadliest of all the solid tumors; the 5‑year survival rate of patients with this disease is ~8%. Previously, high‑throughput sequencing has led to the discovery of novel small non‑coding RNAs, also known as transfer RNA‑derived fragments (tRFs). Studies have suggested that tRFs may be novel biomarkers for certain diseases. However, the expression of tRFs in pancreatic cancer has yet to be characterized. In the present study, the expression levels of tRFs observed in clinical pancreatic cancer samples were analyzed, quantitative PCR (qPCR) was performed to validate the tRFs expression levels and bioinformatics predictions were analyzed. The results revealed that the pancreatic cancer samples screened out a total of 48 tRFs and transfer RNA halves (tiRNAs). There were four tRFs and tiRNAs selected for qPCR validation; the findings were consistent with the sequencing results. Bioinformatic predictions revealed that AS‑tDR‑000064 was predicted to have 2,450 target genes; AS‑tDR‑000069 was predicted 445 target genes; AS‑tDR‑000102 was predicted 746 target genes; and AS‑tDR‑001391 was predicted 216 target genes. Gene Ontology (GO) analyses demonstrated that the target genes of AS‑tDR‑000064 were mostly enriched in ‘the regulation of cellular processes’ (Biological Process), ‘the synapses’ (Cellular Component) and ‘enzyme binding’ (Molecular Function). The target genes of AS‑tDR‑000069 were mostly enriched in ‘signaling’ (Biological Process), ‘the plasma membrane’ (Cellular Component) and ‘phosphatidylinositol 3‑kinase (PI3K) binding’(Molecular Function), the target genes of AS‑tDR‑000102 were mostly enriched in ‘axon development’ (Biological Process), ‘the synapse’ (Cellular Component) and ‘sequence‑specific DNA binding’ (Molecular Function) and the target genes of AS‑tDR‑001391 were mostly enriched in ‘the neuromuscular processes’ (Biological Process), the neurons’ (Cellular Component) and ‘PDZ domain binding’ (Molecular Function). The Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed that the target genes of AS‑tDR‑000064 were mostly enriched in ‘the Ras signaling pathway’, the target genes of AS‑tDR‑000069 were mostly enriched in ‘the cancer pathways’, the target genes of AS‑tDR‑000102 were mostly enriched in ‘axon guidance’ and the target genes of AS‑tDR‑001391 were mostly enriched in ‘the PI3K/protein kinase‑B signaling pathway’.

Background/Aim: Over the past two decades, several advances have been made in the management of patients with hepatocellular carcinoma (HCC) and portal vein tumor thrombosis (PVTT). Yttrium-90 ( ⁹⁰ Y) radioembolization has recently been made a treatment option for patients with HCC and PVTT. However, there is still a need to systematicly evaluate the outcomes of ⁹⁰ Y radioembolization for HCC and PVTT. We aimed to assess the safety and effectiveness of ⁹⁰ Y radioembolization for HCC and PVTT. We performed a systematic review of clinical trials, clinical studies, and abstracts from conferences that qualified for analysis. Materials and Methods: PubMed, EMBASE, Cochrane Database of Systematic Review, CINAHL, and the "gray" literature (Google Scholar) were searched for all reports (1991-2016) related to ⁹⁰ Y radioembolization for HCC and PVTT. Results: A total of 14 clinical studies and three abstracts from conferences including 722 patients qualified for the analysis. The median length of follow-up was 7.2 months; the median time to progression was 5.6 months, and median disease control rate was 74.3%. Radiological response data were reported in five studies, and the median reported value of patients with complete response, partial response, stable disease, and progressive disease were 3.2%, 16.5%, 31.3%, and 28%, respectively. The median survival was 9.7 months for all patients, including the median overall survival (OS) were 12.1, 6.1 months of Child-Pugh class A and B patients, and the median OS were 6.1, 13.4 months of main and branch PVTT patients, respectively. The common toxicities were fatigue, nausea/vomiting, abdominal pain, mostly not requiring medical intervention needed no medication intervention. Conclusions: ⁹⁰ Y radioembolization is a safe and effective treatment for HCC and PVTT.

Early studies have indicated that insulin‑like growth factor II mRNA binding protein 3 (IGF2BP3/IMP3) may affect the progression of hepatocellular carcinoma (HCC); however, the detailed underlying mechanisms, particularly its linkage to tight junction protein‑mediated cell invasion, remain unclear. The present study revealed that IGF2BP3 increased HCC cell invasiveness by suppressing zonula occludens‑1 (ZO‑1) expression, via direct binding to the 3' untranslated region (3'‑UTR). Analysis of the molecular mechanisms demonstrated that IGF2BP3 binds to the overlapping targets of IGF2BP3‑RNA cross‑linkage and microRNA (miR)191‑5p targeting sites, and promotes the formation of an miR191‑5p‑­induced RNA‑induced silencing complex. The knockdown of IGF2BP3 or the addition of a miR‑191‑5p inhibitor decreased cellular invasiveness and increased ZO‑1 expression. Analysis of the human HCC database also confirmed the association between IGF2BP3 and HCC progression. Collectively, these preclinical findings suggest that IGF2BP3 increases HCC cell invasiveness by promoting the miR191‑5p‑induced suppression of ZO‑1 signaling. This newly identified signaling effect on small molecule targeting may aid in the development of novel strategies with which to inhibit HCC progression more effectively.