No abstract

BTG2 (B cell translocation gene 2) is downregulated in several human tumors and has been known as a tumor suppressor in carcinogenesis of thymus, prostate, kidney, and liver. However, little is known about the role BTG2 plays in gastric adenocarcinoma. In the present study, we intended to investigate the influence of BTG2 on the growth, proliferation, apoptosis, invasion and cell cycle of the gastric cancer cell lines SGC7901 and MKN45. BTG2 cDNA was insected into a constitutive vector pcDNA3.1 followed by transfection in gastric cancer cell line MKN45 and SGC7901 by using liposome. Then stable transfectants were selected and appraised. The apoptosis and cell cycles of these transfectants were analyzed by using flow cytometric assay. The growth and proliferation were analyzed by cell growth curves and colony-forming assay, respectively. The invasion of these clones was analyzed by using cell migration assay. MKN-BTG2 (MKN45 with stable transfection of BTG2 gene) and SGC-BTG2 (SGC7901 with stable transfection of BTG2 gene) grew slower than their control groups, respectively. The cell counts of MKN-BTG2 in the fourth, fifth, sixth and seventh days were significantly fewer than those of control groups (P < 0.05). Those of SGC-BTG2 in the fourth fifth, sixth and seventh days were significantly fewer than those of control groups too (P < 0.05). Cell cycle analysis showed that proportions of MKN-BTG2 and SGC-BTG2 cells in G0-G1 and S were different significantly with those of their control groups, respectively (P < 0.05). The apoptosis rate of MKN-BTG2 was significantly higher than those of control groups (P < 0.05). Results of colony-forming assay showed that the colon formation rates of MKN-BTG2 and SGC-BTG2 were lower than those of their control groups (P < 0.05). The results of cell migration assay showed that the cell migration rates of MKN-BTG2 and SGC-BTG2 were not significantly different with those of their control groups (P > 0.05). BTG2 can restrain the growth and proliferation of gastric cancer cells powerfully. It can reduce some malignant phenotype of these tumor cells. But it could not impact the ability of invasion of gastric cancer cells, so could not restrain the metastasis of gastric cancer. In gastric cancer, BTG2 could be thought as a tumor-inhibiting gene in some distance, so the gene could be a potential target of gene therapy.

The upregulation or mutation of C-MYC has been observed in gastric, colon, breast, and lung tumors and in Burkitt’s lymphoma. However, little is known about the role C-MYC plays in gastric adenocarcinoma. In the present study, we intended to investigate the influence of C-MYC on the growth, proliferation, apoptosis, invasion, and cell cycle of the gastric cancer cell line SGC7901 and the gastric cell line HFE145. C-MYC cDNA was subcloned into a constitutive vector PCDNA3.1 followed by transfection in normal gastric cell line HFE145 by using liposome. Then stable transfectants were selected and appraised. Specific inhibition of C-MYC was achieved using a vector-based siRNA system which was transfected in gastric cancer cell line SGC7901. The apoptosis and cell cycles of these clones were analyzed by using flow cytometric assay. The growth and proliferation were analyzed by cell growth curves and colony-forming assay, respectively. The invasion of these clones was analyzed by using cell migration assay. The C-MYC stable expression clones (HFE-Myc) and C-MYC RNAi cells (SGC-MR) were detected and compared with their control groups, respectively. HFE-Myc grew faster than HFE145 and HFE-PC (HFE145 transfected with PCDNA3.1 vector). SGC-MR1, 2 grew slower than SGC7901 and SGC-MS1, 2 (SGC7901 transfected with scrambled control duplexes). The cell counts of HFE-Myc in the third, fourth, fifth, sixth, and seventh days were significantly more than those of control groups (P < 0.05). Those of SGC-MR1, 2 in the fourth, fifth, sixth, and seventh days were significantly fewer than those of control groups (P < 0.05). Cell cycle analysis showed that proportions of HFE-Myc and SGC-MR cells in G0–G1 and G2–M were different significantly with their control groups, respectively (P < 0.05). The apoptosis rate of HFE-Myc was significantly higher than those of control groups (P < 0.05). Results of colony-forming assay showed that the colony formation rate of HFE-Myc was higher than those of control groups; otherwise, the rate of SGC-MR was lower than those of their control groups (P < 0.05). The results of cell migration assay showed that there were no significant differences between experimental groups and control groups (P > 0.05). In conclusion, C-MYC can promote the growth and proliferation of normal gastric cells, and knockdown of C-MYC can restrain the growth and proliferation of gastric cancer cells. It can induce cell apoptosis and help tumor cell maintain malignant phenotype. But it can have not a detectable influence on the ability of invasion of gastric cancer cells.

At a high CO concentration (>20 mg x L(-1)), cell growth and proliferation are inhibited in a dosage-dependent manner. Increase in cell proliferation and in malignant conversion of the cellular phenotype is observed in cells cultured chronically with CO. COX-2 mRNA expression decreases significantly, while human mitochondrial cytochrome C oxidase subunit IImRNA expression increases significantly in HIEC treated with CO. CO also has a direct effect on the contractility of Guinea pig colonic smooth muscle cells.

Anterior tibial plateau fracture is fairly common. This study was aimed at introducing a type of severe anterior tibial plateau fracture (anterior tibial plateau fracture-dislocation) and evaluating its clinical characteristics and treatment strategies. In this study, 18 patients with severe anterior tibial plateau fracture (study group) were enrolled between November 2006 and August 2014, and their data were compared with those of 21 patients treated for normal Schatzker type VI tibial plateau fracture (control group) between January 2010 and August 2014. At the last follow-up, bony union had been achieved in both groups. The incidence of ligament injury was higher in the case of anterior tibial plateau fracture than control group. The average range of motion in the study group was 0.56 to 109 degrees, while that in the control group was 1.81 to 117 degrees. The average Hospital for Special Surgery scores and Lysholm scores in the study group were significantly lower than those in the control group. Further, the incidence of postoperative complications and reduction loss were higher for anterior tibial plateau fracture cases than for normal Schatzker type VI fracture. Our findings also showed a significantly higher rate (22.2%) of popliteal artery injury in the study group than in the control group. Anterior tibial plateau fracture-dislocation is a special type of Schatzker type VI fracture with very low incidence and most commonly characterized by the anterior subsidence of the tibial component, irreducible dislocation of the knee joint, and varying degrees of neurovascular and knee-joint peripheral ligaments injuries, as well as high incidence of complications during fixation surgery. The treatment of anterior tibial plateau fracture-dislocation is challenging even for experienced surgeons.