The dysregulation of miR-663a is frequently observed in many human cancers. However, the functional role and precise mechanism of miR-663a have been controversial in hepatocellular carcinoma (HCC) and need to be studied in depth. The expression of miR-663a was detected in human cell lines and HCC tissues by quantitative RT-PCR (qRT-PCR), and data from the Cancer Genome Atlas (TCGA). Cell proliferation was investigated using MTS, EdU, colony formation assays, and xenograft animal experiments, and the cell invasion capacity was evaluated using the transwell assay. The target gene of miR-663a was identified by qRT-PCR, Western blot, and dual-luciferase reporter assays. The clinicopathological features of miR-663a and the correlation between miR-663a and TGF-β1 expression were also investigated in the clinical samples of HCC. miR-663a was significantly downregulated in HCC cells relative to immortal normal liver cells, as indicated using qRT-PCR, and the lower expression of miR-663a was also confirmed in HCC tissue samples and the data from TCGA. The expression of miR-663a in HCC tissue samples was statistically significantly associated with size and the number of tumors. In addition, the upregulation of miR-663a inhibited the proliferation and invasion of HCC cells in vitro. Further study showed that miR-663a directly targeted transforming growth factor beta 1 (TGF-β1) to suppress HCC invasion, and that the inhibitory effect of miR-663a on cell invasion could be regulated by TGF-β1. In vivo studies showed that miR-663a significantly inhibited tumor growth. A negative correlation between miR-663a and TGF-β1 expression was also confirmed from the clinical samples of HCC. miR-663a acts as a tumor suppressor and exerts a substantial role in inhibiting the proliferation, invasion, and tumorigenesis of HCC by regulating TGF-β1 in vitro and in vivo. These observations indicate that miR-663a may be a suitable diagnostic, therapeutic, and prognostic target for the treatment of HCC.

SGI‑1027, a novel class of relatively stable, highly lipophilic quinoline‑based small‑molecule inhibitors of DNA methyltransferase enzymes (DNMTs), is able to inhibit DNMTs activity, and reactivate tumor suppressor genes. However, the potential anticancer mechanisms of SGI‑1027 on human hepatocellular carcinoma (HCC) cells are still not clearly understood. Thus, the objective of the present study was to clarify the inhibitory effect of SGI‑1027 on the cell cycle and apoptosis of the Huh7 cell line. The results revealed that treatment with SGI‑1027 resulted in a significant dose‑dependent decrease in cell viability. Flow cytometric analysis identified that a 24 h treatment of SGI‑1027 resulted in cell apoptosis, and typical apoptotic nucleic alterations were observed with fluorescence microscopy following terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling staining. Immunoblot analysis further demonstrated that SGI‑1027 downregulated the expression of B cell lymphoma‑2 and upregulated the expression of Bcl‑associated X protein. However, no significant alterations of the cell cycle phases were observed. Overall, it is demonstrated that SGI‑1027 causes cell apoptosis via the mitochondrial‑mediated pathway, which advances current understanding of the molecular mechanisms of SGI‑1027 in HCC management.

Huaier aqueous extract, the main active constituent of Huaier proteoglycan, has antihepatocarcinoma activity in experimental and clinical settings. However, the potential and associated antihepatoma mechanisms of Huaier extract are not yet fully understood. Therefore, in this study, we aimed to elucidate the inhibitory proliferation effect of Huaier extract on apoptosis and cycle of HepG2 and Bel-7402 cells. Our data demonstrated that incubation with Huaier extract resulted in a marked decrease in cell viability dose-dependently. Flow cytometric analysis showed that a 48h treatment of Huaier extract caused cell apoptosis. Typical apoptotic nucleus alterations were observed with fluorescence microscope after Hoechst staining. Immunoblot analysis further demonstrated that Huaier extract activated caspase 3 and PARP. Additionally, Huaier extract inhibited the activity of p-ERK, p-p38, and p-JNK in terms of MAPK. Furthermore, Huaier extract induced HCC cells arrest in S phase and decreased the cycle related protein expression of β-catenin and cyclin D1. Studies with JNK specific inhibitor, SP600125, showed that Huaier extract induced S phase arrest and decreased β-catenin and cyclin D1 expression via JNK signaling pathway. In conclusion, we verify that Huaier extract causes cell apoptosis and induces hepatocellular carcinoma cells arrest in S phase via JNK pathway, which advances our understanding on the molecular mechanisms of Huaier extract in hepatocarcinoma management.

Single-incision laparoscopic cholecystectomy (SILC) is the result of the ongoing trend to minimally invasive of laparoscopy, but some surgeons thought that the SILC can increase the risk of bile duct injure or bile spillage, and the single-incision robotic cholecystectomy (SIRC) can overcome the drawbacks of SILC. Some articles described that the SIRC had longer operative time and more cost than SILC. The advantages and disadvantages of SIRC have still not been extensively studied. We aimed to investigate the outcomes of SIRC compared to SILC and evaluate the safety and feasibility of SIRC. To find relevant studies, the electronic databases PubMed, MEDLINE, The Cochrane Library, and EMBASE were searched to seek information in English literature from 2011 to 2017. Studies comparing SIRC to SILC, for any indication, were included in the analysis. This systematic review and meta-analysis were performed with RevMan Version 5.3. Six comparative studies (n = 633 patients) were included in our analysis. The data showed that the SIRC and SILC had equivalent outcomes for operative time [mean difference (MD) = 17.32, 95% confidence interval (CI): −8.93–43.57, P = .20], intraoperative complications [odd ratio (OR) = 0.48, 95% CI: 0.17–1.39, P = .18], postoperative complications (OR = 0.62, 95% CI: 0.21–1.86, P = .39), hospital stay (MD = −0.01, 95% CI: −0.21–0.19, P = .90), readmissions rate (OR = 0.70, 95% CI: 0.09−5.63, P = .74), and conversion rate (OR = 0.52, 95% CI: 0.14–1.96, P = .33), but total cost was statistically significant (MD = 3.7, 95% CI: 3.61–3.79, P < .00001). SIRC is a safe and feasible procedure for cholecystectomy, and the operative time is same as SILC, but the total cost of SIRC is significantly higher than SILC.