Celecoxib attenuates hepatocellular proliferative capacity during hepatocarcinogenesis by modulating a PTEN/NF-κB/PRL-3 pathway.

Although the efficacy of celecoxib on various cancer cell behaviors, including aberrant proliferation, in cultured hepatocellular carcinoma (HCC) cells has been demonstrated, whether celecoxib regulates cell proliferation by targeting PRL-3-associated signaling transduction during hepatocarcinogenesis has been incompletely studied. Here, we investigate the anti-proliferative efficacy of celecoxib in a rapid HCC mouse model established by hydrodynamic transfection of activated AKT and c-Met proto-oncogenes. The results show that celecoxib is effective at delaying the malignant transformation of hepatocytes by reducing the protein expression of Ki67, Cyclin D1 and c-Myc in the AKT/c-Met HCC-bearing mice.

Celastrol delays hepatic steatosis and carcinogenesis in a rapid AKT/c-Met-transfected hepatocellular carcinoma model suppressing fatty acid synthase expression and AKT/ERK phosphorylation.

Although the suppressing effects of celastrol on hepatocellular carcinoma (HCC) have been demonstrated, evidence for the targeting of fatty acid synthetase (FASN) in the development of HCC by celastrol is still rare. In this study, the effect of celastrol on a rapid HCC model featuring co-activation of AKT/c-Met oncogenes in mice was studied. The effect of celastrol on the alpha-fetoprotein level in the liver and serum was also investigated.

Bioinformatics investigation of therapeutic mechanisms of Xuesaitong capsule treating ischemic cerebrovascular rat model with comparative transcriptome analysis.

Background: Xuesaitong soft capsule (XST) which consists of panax notoginseng saponin (PNS) has been used to treat ischemic cerebrovascular diseases in China. The therapeutic mechanism of XST has not been elucidated yet from prospective of genomics and bioinformatics.

Methods: A transcriptome analysis was performed to review series concerning middle cerebral artery occlusion (MCAO) rat model and XST intervention after MCAO from Gene Expression Omnibus (GEO) database.