miR-181c inhibits glycolysis by targeting hexokinase 2 in cancer-associated fibroblasts / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the role of miR-181c in glycolysis of cancer-associated fibroblasts (CAFs) and explore the mechanism.</p><p><b>METHODS</b>Human lung CAFs and normal fibroblasts (NFs), isolated from fresh human lung adenocarcinoma tissue specimens by primary culture of tissue explants, were transfected with a miR -181c mimics, a miR-181c inhibitor, a siRNA siRNA-HK2 or the vector HK2-vector via Lipofectamine(TM) 2000. Quantitative real-time PCR was used to analyze the changes in miR-125b expression in the transfected cells; hexokinase-2 (HK2) protein expression in the cells was detected using Western blotting, and the cellular glucose uptake was assessed with 2-NBDG. Lactate production in the cells was examined and expression of HK2 mRNA was detected with dual luciferase reporter gene assay.</p><p><b>RESULTS</b>No obvious difference was found in the cell morphology between CAFs and NFs. Compared with the NFs, the CAFs showed obviously increased glucose uptake, lactate production and HK2 protein expression with decreased expressions of the miR-181 family (P<0.05). Transfection with the miR-181 inhibito- rsignificantly increased glucose uptake, lactate production and HK2 protein expression in the NFs. In CAFs, transfection with the miR-181 mimics caused significantly lowered glucose uptake, lactate production and HK2 protein expression of. Knockdown of endogenous HK2 by siRNA abolished miR-181 mimics-mediated decrease of glucose uptake and lactate production in CAFs, while transfection with miR-181 mimics suppressed HK2 overexpression-induced enhancement of glucose uptake and lactate production in NFs.</p><p><b>CONCLUSION</b>Transfection with miR-181 mimics can suppress glycolysis in CAFs by inhibiting HK2 expression.</p>

Cationic liposomes complexed to plasmids encoding endostatin and angiostatin inhibit lewis lung cancer in mice model / 肿瘤研究与临床

Objective To evaluate the inhibitory effect of cationic Liposomes complexed to plasmids encoding endostatin and/or angiostatin on the growth and metastasis of Lewis lung cancer in mice model. Methods C57BL/6j mice were established as mice model. Cationic liposome complexed plasmids encoding angiostatin and endostatin were administrated intratumorally to inhibit the growth and metastasis of the implanted tumor. The size change of the tumor; metastasis in lung, the activity, nourishment, survival period of the mice were observed to evaluate the function of cationic liposome complexed plasmids. Results The treatment group could inhibit the growth and metastasis of the implanted tumor. Comparing with control group, they showed significance in tumor size, metastasis in lung and survival period of the mice (P