Background: The mTOR pathway is vital for homeostasis, metabolism, cancer transplantation and regeneration in the liver. The aim of this study is to use a bibliometric method to reveal current research hotspots and promising future trends in mTOR signaling in liver diseases. Methods: Publications were searched and downloaded from the Web of Science Core Collection (WOSCC) Database. CiteSpace, Carrot2, and VOSviewer programs were utilized to analyze the contribution of various countries/regions, institutes, and authors; and to reveal research hotspots and promising future trends in this research area.Results: Until May 21, 2019, a total of 2,232 papers regarding mTOR signaling pathway in liver disease were included, and each paper was cited 23.21 times on average. The most active country was the USA. 5 landmark articles with centrality and burstiness were determined by co-citation analysis. Research hotspots included "liver transplantation" "hepatic stellate cell proliferation" "NAFLD" "therapy of HCC". Moreover, six key clusters were discovered during the procedure of "clustering", including "liver transplantation" "protein synthesis" "mTOR inhibitor" "following early cyclosporine withdrawal" "srebp-1 activation", and "hepatocellular cancer". Conclusions:Various scientific methods were applied to reveal scientific productivity, collaboration, and research hotspots in the mTOR signaling pathway in liver disease. Liver transplantation, hepatic stellate cell proliferation, non-alcoholic fatty liver disease (NAFLD), therapy of hepatocellular carcinoma (HCC), cell growth and autophagy, are research hotspots and are likely to be promising in the next few years. Further studies in this field are needed.

BackgroundThe physiological regulatory functions of circRNAs have become a topic of intensive research in recent years. Increasing evidence supports a significant role of circRNAs during cancer initiation and progression, including hepatocellular carcinoma (HCC).Materials and MethodsA bioinformatics analysis from three independent Gene Expression Omnibus (GEO) databases was performed to profile and screen the dysregulated circRNAs in HCC. RT-qPCR was used to examine the expression level of circUBAP2 in HCC and adjacent non-tumor tissues. Then, proliferation assays (CCK8 and colony formation) and migration assays (transwell and wound healing) were performed to examine effect of circUBAP2 in vitro. Immunoprecipitation, RNA pulldown, FISH, and dual-luciferase reporter assay was conducted to explore the circUBAP2-related mechanism for regulating HCC progression. Moreover, a mouse xenograft model and a mouse lung metastasis model confirmed the effect of circUBAP2 in vivo.ResultsIn this study, we found a novel circRNA: circUBAP2, which was identified by bioinformatics analysis. Among 91 HCC patients, circUBAP2 was significantly upregulated in HCC tissues, and negatively correlated with aggressive clinical characteristics and prognosis. Functional assays demonstrated that circUBAP2 promoted cell proliferation, colony formation, migration, and invasion in vitro. Moreover, circUBAP2 enhanced tumor growth and pulmonary metastasis in vivo. Mechanistically, circUBAP2 acts as a competing endogenous RNA (ceRNA) for miR-194-3p, a tumor suppressor in HCC. We confirmed that MMP9 was direct target for miR-194-3p, which was regulated by circUBAP2.ConclusionCircUBAP2 plays a significant role in promoting HCC via the miR-194-3p/MMP9 pathway and could serve as a promising prognostic biomarker and novel therapeutic target for HCC patients.

BackgroundOver the last decades, the number of patients diagnosed with thyroid carcinoma has been increasing, highlighting the importance of comprehensively evaluating causes of death among these patients. This study aimed to comprehensively characterize the risk of death and causes of death in patients with thyroid carcinoma.MethodsA total of 183,641 patients diagnosed with an index thyroid tumor were identified from the Surveillance, Epidemiology, and End Result database (1975–2016). Standardized mortality rates (SMRs) for non-cancer deaths were calculated to evaluate mortality risk and to compare mortality risks with the cancer-free US population. Cumulative mortality rates were calculated to explore the factors associated with higher risk of deaths.ResultsThere were 22,386 deaths recorded during follow-up, of which only 31.0% were due to thyroid cancer and 46.4% due to non-cancer causes. Non-cancer mortality risk among patients with thyroid cancer was nearly 1.6-fold (SMR=1.59) that of the general population. Cardiovascular diseases were the leading cause of non-cancer deaths, accounting for 21.3% of all deaths in thyroid cancer patients. Non-cancer causes were the dominant cause of death in thyroid cancer survivors as of the third year post-diagnosis. We found that males with thyroid cancer had a higher risk of all-cause mortality compared with females. The risk of suicide was highest in the first post-diagnostic year (<1 year: SMR=1.51). The long-term risk of Alzheimer’s disease was notably increased in thyroid cancer patients (>5 years: SMR=8.27).ConclusionNon-cancer comorbidities have become the major risks of death in patients with thyroid tumor in the US, as opposed to death from the tumor itself. Clinicians and researchers should be aware of these risk trends in order to conduct timely intervention strategies.