A Meta-analysis of the efficacy and safety of Kanglaite injection combined with chemotherapy in the treatment of pancreatic cancer

Objective:To investigate the efficacy and safety of Kanglaite injection(KLT)combined with chemotherapy in the treatment of pancreatic cancer.Methods:PubMed,EMBASE,the Cochrane Library,China National Knowledge Infrastructure(CNKI),Wanfang Database,VIP Data,and Chinese Biomedical Database(CBM)were searched to get the studies about KLT plus chemotherapy for pancreatic cancer(from established to May 2019).Data extraction and bias risk assessment were carried out by two authors independently according to the retrieval method.RevMan(version 5.3)were employed for data analysis.Results:A total of 151 literatures were retrieved and 11 literatures were finally included.A total of 614 patients were included,including 308 in the treatment group and 306 in the control group.The results of meta-analysis showed that compared with chemotherapy alone,KLT combined with chemotherapy could improve the effective rate[Porr=0.0009,OR=1.96,95%CI(1.32,2.92)]and disease control rate[Pdcr<0.00001,OR=2.53,95%CI(1.76,3.62)],improve KPS score[P<0.00001,OR=3.59,95%CI(2.00,6.44)]and body mass indexes[P=0.0003,OR=3.45,95%CI(1.78,6.69)],prolong progression free survival(PFS)and overall survival(OS),reduce the rate of myelosuppression[P=0.03,OR=0.54,95%CI(0.30,0.95)],but could not reduce the occurrence of neurotoxicity[P=0.49,OR=0.80,95%CI(0.42,1.51)]and digestive tract reaction[P=0.51,OR=0.83,95%CI(0.48,1.44)].Conclusion:KLT combined with chemotherapy can improve the curative effect of pancreatic cancer,improve the quality of life of patients,prolong the survival of patients,and reduce the incidence of bone marrow suppression.However,due to the limitation of the quality and quantity of included literatures,this conclusion needs to be verified by high-quality study.

KRT17 Promotes the Activation of HSCs via EMT in Liver Fibrosis

Background and Aims:Although activation of hepatic stellate cells(HSCs)plays a central role in the development of liver fibrosis,the mechanism underlying the activation of HSCs remains unclear.Keratin 17(KRT17),a member of the intermediate filament family,can regulate tumor cell proliferation and migration.The current study aimed to elucidate the role of KRT17 in the activation of HSCs and the mechanisms underlying liver fibrosis.Methods:The expression of KRT17 was determined using immunohistochemistry in tissue microarray.Western blotting and qRT-PCR assays were used to determine the KRT17 expression in fibrotic liver tissues obtained from human subjects and mice.LX-2 cells were treated with TGF-β1 recombinant protein and adipocyte differentiation mixture(MDI)mix to induce and reverse LX-2 cell activation,respectively,in order to explore the correlation between KRT17 and HSC activation.Additionally,cell proliferation and migration abilities of LX-2 cells transfected with KRT17-overexpressing plasmid or small interfering RNA were determined using CCK-8,flow cytometry,Transwell,and wound healing assays.Finally,rescue assay was used to explore the role of KRT17 in HSC activation and epithelial-mesenchymal transition(EMT).Results:The expression of KRT17 was higher in the hu-man and mouse fibrotic liver tissues than in healthy liver tissues,and it was positively correlated with HSC activa-tion.Upregulated KRT17 enhanced proliferation,migration,HSC activation and EMT in LX-2 cells,while knockdown of KRT17 reversed these effects.TGF-β1 recombinant protein accelerated KRT17-mediated EMT,HSC activation and proliferation,while TGF-β1 inhibitor counteracted the effect of KRT17 in vitro.Conclusions:KRT17 promoted HSC activation,proliferation and EMT in hepatic fibrosis probably via TGF-β1 signaling,and KRT17 might serve as a therapeutic target for the treatment of liver fibrosis.