The present research was major in investigating the regulation association among hsa_circ_0101432 (has_circ_RPPH1), miR-1258, miR-622 and MAPK1 in hepatocellular carcinoma (HCC), and we explored the mechanism underlying pathogenesis of HCC. Microarray analysis was employed to detect hsa_-circ_0101432 expression in HCC. Hsa_circ_0101432 was verified as a circRNA by testing divergent primers and RNase R. And qRT-PCR was performed to determine the expression of hsa_circ_0101432, miR-1258, miR-622 and MAPK1 mRNA. Furthermore, miRanda predicted that mRNAs targeted miR-1258 and miR-622. CCK-8 assay, colony formation assay, flow cytometry as well as transwell assay were performed to detect cell viability, proliferation, apoptosis and invasive ability, respectively. Xenograft in nude mice was applied to observe tumor growth in vivo. Up-regulated hsa_circ_0101432 and downregulated miR-1258 and miR-622 were detected in HCC while Hsa_circ_0101432 enhanced expression of MAPK1 mRNA by targeting miR-1258 and miR-622. Knocking down hsa_circ_0101432 or overexpressing miR-1258 and miR-622 inhibited proliferation and invasive ability of HCC cell and promoted cell apoptosis. Hsa_circ_0101432 was confirmed to promote tumor growth via inhibiting miR-1258 and miR-622 expression and promoting MAPK1 mRNA expression by in vivo experiment. Hsa_circ_0101432 inhibited HCC cell apoptosis, promoted cell proliferation, invasive ability and HCC tumor growth by targeting miR-1258 and miR-622 and upregulating MAPK1 mRNA expression.

Accumulating evidence has demonstrated that the aberrant expression of microRNAs (miRs or miRNAs) may contribute to the initiation and progression of various types of human cancer and may also constitute biomarkers for cancer diagnosis and therapy. However, the specific function of miR‐9 in hepatocellular carcinoma (HCC) remains unclear, and the mechanisms that underlie HCC are incompletely understood. Here, we report that miR‐9 expression was significantly decreased in clinical tumor tissue samples, as well as in a cohort of HCC cell lines. In addition, it was demonstrated that overexpression of miR‐9 suppressed the proliferative and migratory capacity of HCC cells and impaired cell cycle progression. Furthermore, high mobility group AT‐hook 2 (HMGA2) was verified as a downstream target gene of miR‐9 using a luciferase reporter assay. Quantitative RT‐PCR and western blotting implicated HMGA2 in the miR‐9‐mediated reduction of HCC cell growth. In vivo, transfection with miR‐9 mimics down‐regulated the expression of HMGA2, thus leading to a dramatic reduction in tumor growth in a mouse xenograft model. These results suggest that miR‐9 may exert critical antitumor effects on HCC by directly targeting HMGA2, and the miR9/HMGA2 signaling pathway may be of use for the diagnosis and prognosis of patients with HCC.

Severe acute pancreatitis (SAP) is a critical disease caused by diffuse hemorrhage of the pancreas and combined with necrosis of surrounding tissues. 1 Conventional symptomatic treatments such as pain relief, gastrointestinal pressure reduction, correction of water and electrolyte and acid-base disorder play an important role in controlling the secretion of gastric juice and pancreatic juice in patients with severe acute pancreatitis, but the therapeutic effect is not ideal. Somatostatin is a kind of peptide hormone, which has an effect on the inhibition of the secretion of growth hormone and gastrointestinal hormone. Studies have shown that early use of somatostatin can alleviate inflammation and improve immune function in SAP patients, but the impact on mortality and morbidity of patients needs further study. 2 Pantoprazole is a new proton pump inhibitor, which can reduce the secretion of gastric acid and pepsin and effectively improve the gastrointestinal PH value of patients, thus blocking the secretion of physiological protease, reducing the secretion of pancreas body, and exerting a high acidsuppressing effect. Pantoprazole can reduce inflammatory cell infiltration and necrosis of acinar cells in SAP patients, which has been shown in a study. 3 Serum levels of C-reactive protein (CRP) and intercellular adhesion molecule-1 (ICAM-1) are important experimental indi-

BackgroundLiver cancer is one of the most common malignancies around the world and one of the major causes of cancer related mortality. The objective of this study was to evaluate the anticancer effect of the natural compound psilostachyin-A on 5-fluorouracil-resistant human liver carcinoma cells and its effects on autophagy, cell cycle, caspase activation, and the ERK/MAPK signaling pathway.Material/MethodsCell Counting Kit 8 (CCK-8) assay was used to evaluate the effects on HepG2 cell viability at different doses of psilostachyin-A. Cell cycle analysis was performed using flow cytometry, and Transwell assay was used to check effects on cell invasion. Transmission electron microscopic studies were done to evaluate autophagy induced by psilostachyin-A, and the western blot method was carried out to evaluate the effects on autophagy and the ERK/MAPK signaling pathway.ResultsCCK-8 assay revealed that the psilostachyin-A reduced the cell viability of HepG2 cancer cells in a dose dependent manner. Psilostachyin-A also reduced the colony forming potential of HepG2 cells, concentration dependently. The IC50 of psilostachyin was found to be 25 μM. The anticancer effects of psilostachyin-A were due to the induction of autophagy which was accompanied by enhancement of LC3B II expression. Psilostachyin also caused cell cycle arrest by enhancing the accumulation of HepG2 cells in the G2/M phase. Transwell assay showed that psilostachyin-A suppressed the invasion of HepG2 cells. The results also showed that psilostachyin-A could block the ERK/MAPK pathway, indicative of the cytotoxic effects of psilostachyin-A on liver cancer.ConclusionsThese preliminary observations suggested that psilostachyin-A might prove beneficial in the treatment of liver cancer.

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