Recently, there has been growing support for the cancer stem cell (CSC) hypothesis, which states that primary tumors are initiated and maintained by a small subpopulation of cancer cells that possess "stem-like" characteristics. CSCs have been identified in many tumor types, including hepatocellular carcinoma (HCC). The dye, Hoechst 33342, has been used to enrich CSCs into a side population. Alternatively, liver CSCs (LCSCs) can be identified by several cell surface antigens, including CD133, CD90, CD44, EpCAM, and CD13. In this review, we summarized the recent evidence regarding LCSC markers and discussed the origin and function of these markers. LCSC markers are essential to identify and isolate these cells, to develop future therapies targeting CSCs, and to predict prognosis and efficacy of these therapies. However, definite LCSC markers are still controversial, because none of these markers is exclusively expressed by LCSCs in HCC. By combining several positive or negative markers, it may be possible to isolate and identify CSC fractions beyond the ability of each individual assay. By grouping LCSC markers according to their cellular origin, the properties of LCSC markers may be better studied and new markers may be found. Lastly, markers could be used to estimate the number of LCSCs and therefore predict outcomes. From our point of view, selecting HCC tissue samples from patients with different prognoses and detecting expression patterns of marker combinations may be a new method to identify new and unique markers.

BackgroundGrowing evidence suggests that the ubiquitin-proteasome system is involved in the pathogenesis and recurrence of hepatocellular carcinoma (HCC); yet, little is known about the role of ubiquitin-conjugating enzyme E2T (UBE2T) in HCC.Materials and methodsUBE2T levels were detected in HCC tissues and hepatoma cell lines using quantitative reserve transcriptase-polymerase chain reaction and Western blot analysis. Next, the changes of phenotypes after UBE2T knockdown or overexpression were evaluated using in vitro methods. Finally, the mechanism of UBE2T in HCC was tested using ex vivo and in vivo methods.ResultsIn the present study, we reported that UBE2T mRNA and protein levels were significantly upregulated in HCC tissues compared to adjacent non-tumor tissues. Additionally, suppression of UBE2T expression inhibited proliferation, colony formation, tumorigenesis, migration, and invasion of hepatoma cells, whereas UBE2T overexpression led to the opposite outcomes. Moreover, suppression of UBE2T expression resulted in an increase in G2/M phase and a decrease in the percentage of cells in G1 phase, which indicated a cell cycle arrest at the G2/M phase. In contrast, the percentage of cells in G2/M phase decreased following UBE2T overexpression. Further study indicated that UBE2T regulated the G2/M transition by modulating cyclin B1 and cyclin-dependent kinase 1.ConclusionTaken together, the findings of the present study uncover biological functions of UBE2T in hepatoma cells, and delineate preliminary molecular mechanisms of UBE2T in modulating HCC development and progression.

Objectives Acute pancreatitis (AP) is a serious gastroenterological condition requiring urgent fluid resuscitation and emergent intensive care. However, the benefit of fluid resuscitation is inconsistent. Therefore, this study aimed to examine the effects of fluid resuscitation on the occurrence of organ failure and mortality in patients with AP. Methods The data were retrospectively extracted from the Medical Information Mart for Intensive Care III 2002–2012 database. The fluid resuscitation and fluid balance were calculated at 12, 24, 36, and 48 hours after intensive care unit admission. Multivariate analysis models were used. Results A total of 317 patients with AP were included. Odds of organ failure increased significantly with increased fluid input at 0 to 12 hours [adjusted odds ratio (aOR), 1.124; 95% confidence interval (CI), 1.015–1.244] and with increased fluid balance at 36 to 48 hours (aOR, 1.184; 95% CI, 1.009–1.389). Odds of in-hospital mortality increased significantly with increased fluid balance at 24 to 36 hours (aOR, 1.201; 95% CI, 1.052–1.371). Odds of 30-day mortality increased significantly with increased fluid balance at 24 to 36 hours (aOR, 1.189; 95% CI, 1.039–1.361). Conclusions Increased fluid balance was associated with increased risk of organ failure and mortality. Increased fluid output may decrease mortality.