Effects of MicroRNA-132 transfection on the proliferation and apoptosis of human liver cancer cells in vitro and in vivo.

OBJECTIVE: To observe the biological role and underlying mechanism of microRNA-132 (miR-132) in liver cancer cell proliferation and apoptosis. METHODS: The expressions of miR-132 in the cancer tissue and their adjacent tissues from 45 liver cancer patients were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The biological effects of miR-132 transfection on human liver cancer MHCC97H cells were assessed by CCK-8 assay, flow cytometry,in vivo experiment in nude mice, and TUNEL test. Western blotting was used to detect the expressions of p-AKT, Survivin, and Caspase 3 in liver cancer cells. Immunohistochemistry was used to detect the positive expressions of Ki-67,Survivin,and Caspase 3 in the xenograft tumors. RESULTS: The expression level of miR-132 was found to be down-regulated in liver cancer tissues compared with the matched adjacent tissues (P<0.05). After transfection,the expression of miR-132 was significantly higher than blank control group and negative control group (P<0.05). The proliferation of liver cancer cells was inhibited significantly by miR-132 transfection (P<0.05). Transfection of miR-132 arrested cells in the G0/G1 phase and triggered apoptosis of MHCC97H cells (P<0.05). After miR-132 transfection,the expression of Caspase 3 was up-regulated, whereas the expressions of p-AKT and Survivin were down-regulated (P<0.05). In addition,the tumor weight in miR-132 transfection group was significantly decreased in comparison with blank control group and negative control group (P<0.05). Apoptosis occurred more frequently in the miR-132 transfection group than in control groups (P<0.05). Compared with the blank control group and negative control group, the miR-132 transfection group had significantly decreased expression of Survivin but increased positive expression of Ki-67 and Caspase 3(P<0.05). CONCLUSIONS: miR-132 is down-regulated in human liver cancer tissues miR-132 transfection can effectively inhibit proliferation and promote apoptosis of MHCC97H cells in vitro and in vivo. Therefore, miR-132 may become a new target in liver cancer treatment.

Treatment selection for gastric cancer with portal hypertension: clinical management.

BACKGROUND: Treatment for gastric cancer with portal hypertension must consider the eradication of the tumor and the change of hemodynamics in portal hypertension (PHT). Few reports have described the surgical procedures and postoperative complications of surgery for gastric cancer associated with PHT. METHODS: The clinical data of 22 patients with PHT undergoing curative surgery for gastric cancer during 5 years were retrospectively analyzed. For 12 patients classified in Child's class A, D2 lymph node (LN) dissection was performed, and 10 patients classified into Child's class B were treated with D1 LN dissection. Surgical treatment included total gastrectomy combined with pericardial devascularization, distal subtotal gastrectomy, distal subtotal gastrectomy combined with splenectomy, and distal subtotal gastrectomy combined with pericardial devascularization with posterior gastric artery and left inferior phrenic artery preserved. A liver biopsy was analyzed in all patients. RESULTS: Postoperative complications developed in 50 % (11/22 patients) and the mortality rate was 9 % (2/22). The rate of postoperative ascites in patients with Child's class A was much lower than in those with Child's class B (P < 0.05). "Operation time," "volume of hemorrhage," "platelet count," and "treatment of PHT" are all risk factors of liver function deterioration. However, there was no significant difference in liver function deterioration rate between patients with Child's class A and Child's class B (P > 0.05). The occurrence rate of complications in patients with PHT was much higher compared to those without with PHT (P < 0.05). CONCLUSIONS: Individualized selection of surgical approaches is crucial for treatment of gastric carcinoma accompanied by PHT. Surgical treatment should be based on preoperative TNM stage, liver function, and degree of PHT.

[Effect of Ginkgo biloba extract on the function of alveolar polymorphonuclear neutrophils in severe acute pancreatitis rats complicated with lung injury].

OBJECTIVE: To explore the effect of Ginkgo biloba extract (GBE) on the function of alveolar polymorphonuclear neutrophils (PMN) in severe acute pancreatitis (SAP) rats complicated with lung injury (LI). METHODS: Forty-eight adult SD rats were randomly divided into three groups, i.e., the sham-operation group, the SAP group, and the GBE treatment group, 16 in each group. The SAP model was successfully induced by retrograde injection of 5% sodium taurocholate solution into the biliopancreatic duct. Rats in the sham-operation group only received flipping of the duodenum. Those in the GBE treatment group received GBE intervention based on SAP model. Equal volume of normal saline was given to rats in the sham-operation group and the SAP group. Rats were sacrificed at 6 and 12 h after operation respectively. The lung tissue was sampled to evaluate the LI score. The wet/dry ratio (W/D) of lung tissues was detected. The activity of myeloperoxidase (MPO) was measured. Alveolar PMN was harvested by bronchoalveolar lavage. The content of neutrophil elastase (NE) in bronchoalveolar lavage fluid (BALF) was measured by enzyme-linked immunoabsorbent assay (ELISA). The percentage of CD11b/CD18 double positive PMN was detected using flow cytometry. The expression of intercellular adhesion molecule-1 (ICAM-1) and NE protein in the lung tissue was detected by Western blot. RESULTS: Compared with the sham-operation group, significant pathologic lesion occurred in the lung tissue of rats in the SAP group; the pathologic LI score, lung tissue W/D ratio, MPO, and NE content in BALF significantly increased, the expression of ICAM-1 and NE in the lung tissue was obviously up-regulated, and the percentage of CD11b/CD18 double positive PMN significantly increased (P < 0.01). Compared with the SAP group, pathological lesion of the lung tissue was obviously attenuated, and the above indices were all significantly declined in the GBE treatment group (P < 0.01). CONCLUSIONS: Expression of ICAM-1 in the lung tissue and the percentage of D11b/ CD18 double positive PMN were up-regulated in SAP rats complicated with LI, resulting in the adherence of PMN to pulmonary vascular endothelial cells, and then activating PMN to release NE and aggravate LI. GBE could alleviate LI through down-regulating the expression ICAM-1 and CD11b/CD18, and hindering the adherence and activation of PMN to pulmonary vascular endothelial cells.