RESUMEN
Hepatocellular carcinoma (HCC) is a frequently occurred malignancy worldwide with a high mortality. The treatment for HCC is still controversial. Emerging evidences have demonstrated that microRNAs (miRs) play a role in HCC. This study aims to investigate the effects of lentiviral-mediated miRNA-26b (miR-26b) on the proliferation and metastasis of HCC cells. The normal hepatic cell line HL-7702 and HCC cell lines HepG2 (without metastatic potential), SMMC-7721 (with low metastatic potential) and MHCC97H (with high metastatic potential) were purchased for our experiment. The lentiviral-mediated miR-26b overexpression (miR-26b-LV) and low expression (sh-miR-26b) were constructed to transfect the cells. The miR-26b expression and expressions of Karyopherin α-2 (KPNA2), matrix metalloproteinase 1 (MMP-1), MMP-7 and MMP-14 were determined by RT-qPCR and western blot analysis. The proliferation and metastasis of transfected HCC cells were detected by MTT and Transwell assay respectively. The miR-26b expressions were decreased significantly in MHCC97H cells. With lentiviral-mediated miR-26b overexpression, the proliferation and migration of HepG2, MHCC97H and SMMC-7721 cells were decreased significantly. The RT-qPCR and western blot analysis results revealed that the mRNA and protein expressions of KPNA2, MMP-1, MMP-7 and MMP-14 were decreased by lentiviral-mediated miR-26b overexpression. All the above indexes in the HepG2, MHCC97H and SMMC-7721 cells treated by sh-miR-26b exhibited opposite trends. These results show that overexpressed miR-26b could inhibit the proliferation and metastasis of HCC cells significantly, which provides a novel target and theoretical foundation for the treatment of HCC.
Asunto(s)
Carcinoma Hepatocelular/genética , Lentivirus/genética , Neoplasias Hepáticas/genética , MicroARNs/genética , Western Blotting , Carcinoma Hepatocelular/terapia , Movimiento Celular/genética , Movimiento Celular/fisiología , Proliferación Celular/genética , Proliferación Celular/fisiología , Regulación Neoplásica de la Expresión Génica/genética , Regulación Neoplásica de la Expresión Génica/fisiología , Células Hep G2 , Humanos , Neoplasias Hepáticas/terapiaRESUMEN
BACKGROUND: The purpose of this study was to investigate the hypoglycemic effect of new biliopancreatic diversion and duodenal-jejunal bypass in Goto-Kakizaki rats and observe effects of the new surgical procedure on the glucose tolerance of GK rats. METHODS: Twenty-four 10-week-old rats (SPF grade) were randomly divided into groups A, B, and C, each with eight rats. Group A underwent duodenal-jejunal bypass, group B underwent modified biliopancreatic diversion, and group C underwent a sham operation. Median rat body weight, fasting blood glucose, OGTT, and blood lipids were measured in fasting 1 week before surgery and 1, 2, 4, and 8 weeks after surgery. Changes in gastric inhibitory polypeptide, glucagon P-like peptide-1, and insulin levels were measured by ELISA 1 week before surgery and 8 weeks after surgery. RESULTS: Rats' mean body weight in groups A and B decreased significantly from 368.025 ± 11.726 and 373.100 ± 9.859 g preoperatively to 345.750 ± 11.403 and 343.260 ± 12.399 g at the early postoperative stage (P < 0.05), and with statistically significant differences compared to the weight of rats in group C (P < 0.05). Comparisons between fasting blood glucose before surgery and 8 weeks after surgery revealed no significant differences between all three groups (P > 0.05). Glucose tolerance in groups A and B decreased from preoperative 21.175 ± 3.684 and 20.820 ± 1.671 mmol/L to postoperative 8.950 ± 0.580 and 10.500 ± 1.509 mmol/L, and both were better than that of group C (P < 0.001). CONCLUSIONS: Both new biliopancreatic diversion and duodenal-jejunal bypass improve glucose tolerance of Goto-Kakizaki rats.