Objective:To investigate effects and underlying me chanisms of miR-199a on prolifer ation of HepG2. Methods:The miR-199a gene was cloned to lentiviral expression vectorpLV-GFP-puro with EGFP by recombining DNA technology,and positive clones were i dentified by DNA sequencing. The 293T cells were cotransfected with lentiviral packaged systems and miR-199a gene plasmid by lipofectinregeant to package the lentiviral partic les.The HepG2 cells were infected with purified recombinant lentivirus. The transfec tion efficiency was assessed under fluores cent micros cope;MTT assay was used to detect cell proliferation;Western Blot was used to analyzae expressions of miR-199A and NF-kB related anti-apoptotic genes(TRAF2,cIAP2,Bfl-1 and cFLIP)in transfected HepG2 cells.Results:The recombinant lentiviral vectors of miR-199a gene were successfully constructed. The virus reached a titer of 1.0.8×108TU/mL after being packaging,purification and concentration. Interestingly,the transfected cells held high expression of miR-199a,which inhibited the pression of miR-199a,cells.ln addition,the transfencted HepG2 cells stablely expressed IkBa,effectively inhibited NF-kB activity,and further suppressed expressions of NF-kB related anti-apoptotic genes(TRAF2.c IAP2,Bfl-1 and cFLIP).Conclusion:The miR-199a recombinant lentiviral vector had been successfully constructed and effectively transfected HepG2 cells, which inhited the proliferation of HepG2 cells . The underlying me chanisms may beinhibit NF-kB activity,and further inhibitexpressions of NF-kB related anti-apoptotic genes by miR-199a.