ABSTRACT
Objective:To establish a colon cancer cell line which overexpressing LINC01018 stably and study its biological characteristics.Methods:The expression of LINC01018 in HCoEpiC and HT-29 cells were detected by real time fluorescence quantitative polymerase chain reaction (qRT-PCR). HT-29 cells were infected with LINC01018 overexpression lentivirus to screen and establish HT-29 cell lines which overexpressing LINC01018 stably. The effect of LINC01018 on the proliferation, invasion and migration of HT-29 cells were detected by cell counting kit-8 (CCK-8) assay and Transwell assay separately. The expression of CDK6 and matrix metalloproteinase-2 (MMP-2) in HT-29 cells was detected by Western blot.Results:The expression of LINC01018 in HT-29 cells was significantly lower than that in the human colonic epithelial cells (HCoEpiC). HT-29-L18 cell lines which overexpressing LINC01018 stably was screened successfully. Overexpression of LINC01018 significantly inhibited the cell proliferation, invasion and migration, and reduced the protein expression of CDK6 and MMP-2 in HT-29 cells.Conclusions:The expression of LINC01018 was decreased abnormally in colon cancer cells. Up-regulation of LINC01018 expression can inhibit the proliferation, invasion and migration of colon cancer cells, which may be related to CDK6 and MMP-2.
ABSTRACT
Objective To explore influence of hypertriglyceridemia on serum NO ET-1 and the grade of the pathology severity in rats with severe acute pancreatitis. Methods 36 SD rats were randomly divided into 2 groups, group A (HLSAP group) , group B (SAP group). Severe acute pancreatitis was constructed by retrograde injection of 5% na-taurocholate. Blood samples were taken from all subjects to measure triglyceride, ET-1 and NO, pancreatic tissue samples were taken from head of pancreas and stained with H. E. , the degree of pancreatic damage was observed according to the point score of Schmidt and Pozsar's methods. Results In group A, the concentration of ET-1 increased more obviously than that in group B at 4 hour and 8 hour period(P ＜0. 05). The concentration of NO declined both in group A and group B at 12 hours period,but it had a great decline in group A. Animals with hyperlipidemia and severe acute pancreatitis developed significantly higher(P ＜0. 05) ET-1 than the animals of the non-hyperlipamic severe acute pancreatit group in 4 hours and 8 hours period. NO declined in group A and group B at 12 hours period, group A have significantly higher(P ＜0. 05) decline than group B in NO. The histological degree of pancreatic damage were significantly higher in group A than that in the group B at all times. Conclusions Mircrocirculation disorder had existed disorder in the early of SAP. Hypertriglyceridemia could incrase ET-1 and NO earlier and higher in severe acute pancreatitis, and then decline in the late stage. Hypertriglyceridemia intensified the pathologichistological degree of pancreatic damage.