BackgroundLong noncoding RNAs (lncRNAs) have been identified as prognostic biomarkers and functional regulators in human cancers. The present study aimed to determine the expressions and functions of an lncRNA, Small Nucleolar RNA Host Gene 16 (SNHG16), in hepatocellular carcinoma (HCC).Patients and methodsSNHG16 expressions were tested by quantitative real-time PCR (qRT-PCR) in HCC cell lines, as well as 43 pairs of HCC tissues and pair-matched healthy hepatic tissues. It was overexpressed in Hep3B and HuH7 cells. The effects of SNHG16 overexpression in HCC in vitro proliferation, 5-fluorouracil (5-FU) chemoresistance, and in vivo tumor growth were tested. A potential microRNA (miRNA) sponge target of SNHG16, hsa-miR-93, was tested by luciferase reporter assay and qRT-PCR. In addition, hsa-miR-93 was upregulated in SNHG16-overexpressed HCC cells to examine its effect on SNHG16-mediated cancer cell functional regulation in HCC.ResultsSNHG16 levels were markedly downregulated in both HCC cell lines and HCC tissues. Lentivirus-mediated SNHG16 overexpression inhibited HCC cell proliferation, 5-FU chemoresistance, and in vivo tumor growth. Hsa-miR-93 was confirmed to be directly sponging on SNHG16. Its upregulation in HCC cells reversed SNHG16 overexpression and induced tumor-suppressing effects in HCC cells.ConclusionOur data demonstrate that SNHG16 plays a critical role in HCC development via functionally sponging hsa-miR-93.

Hepatocellular carcinoma is the sixth most common cancer and gives rise to numerous deaths around the world every year. However, the molecular mechanism that controls hepatocarcinogenesis remains largely unknown. Here we found out an uncharacterized long noncoding RNA named lncAKHE. We found that lncAKHE was highly expressed in hepatocellular carcinoma tissues. lncAKHE depletion remarkably impaired the abilities of cell proliferation, migration, and invasion in hepatocellular carcinoma while promgoogoting cell apoptosis. Moreover, higher expression level of lncAKHE in hepatocellular carcinoma tissues was associated with more clinical severity and lower survival rates. Mechanistically, lncAKHE cooperated with YEATS4 to enhance the activation of NOTCH2 signaling which is usually abnormally upregulated in hepatocellular carcinoma. In conclusions, our study showed that lncAKHE may promote tumor progression in HCC and serve as a novel target for HCC treatment.

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BackgroundElevated plasma fibrinogen levels have been associated with tumor progression in several malignancies. Our study aims to characterize the clinical significance of elevated plasma fibrinogen levels in patients with hepatocellular carcinoma (HCC).Materials and methodsRelevant published articles were systematically searched in electronic databases including PubMed, Embase, and Web of Science. The pooled differences in plasma fibrinogen levels among HCC, cirrhotic, and control groups were expressed as weighted mean differences (WMDs) and their corresponding 95% CIs. The associations between elevated fibrinogen and overall survival (OS) and disease-free survival (DFS)/recurrence-free survival (RFS) were expressed as HRs and their 95% CIs, whereas the associations between elevated fibrinogen and various types of clinical characteristic of patients with HCC were expressed as ORs and their corresponding 95% CIs.ResultsResults showed that the plasma fibrinogen levels in patients with HCC were not significantly different than that in healthy controls (WMD = 0.50, 95% CI = [−0.82, 1.82], P = 0.457) or patients with cirrhosis (WMD = −0.62, 95% CI = [−1.56, 0.33], P = 0.200). However, our results showed that compared to those with normal levels, patients with HCC and elevated plasma fibrinogen levels showed poorer OS (HR = 2.08, 95% CI = [1.67, 2.59], P < 0.0001) and DFS/RFS (HR = 1.90, 95% CI = [1.52, 2.37], P < 0.0001). Results of trial sequential analysis of the OS indicated that currently available studies were sufficient to validate the negative prognostic value of elevated plasma fibrinogen in patients with HCC. Clinicopathological analyses showed that high plasma fibrinogen levels were associated with tumor progression as indicated by advanced tumor stage, larger tumor size, increased tumor number, and the presence of vascular invasion.ConclusionElevated plasma fibrinogen levels are associated with poor prognosis and advanced tumor progression. Plasma fibrinogen may serve as a negative prognostic biomarker in patients with HCC.

Objectives To investigate, using three-dimensional power Doppler ultrasound (3D-PDU), alterations in cervical intratumoral vascularization during and after radiotherapy. Methods