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Chinese Journal of Hepatobiliary Surgery ; (12): 444-448, 2022.
Article in Chinese | WPRIM | ID: wpr-956981

ABSTRACT

Objective:To explore the molecular mechanism that how microRNA-122 (miR-122) inhibitis the growth of hepatocellular carcinoma associated with hepatitis B virus (HBV) infection.Methods:mRNA and protein expression of miR-122 and N-myc downstream regulatory gene 3 (NDRG3) were detected in hepatocellular carcinoma cells HepG2, HepG2.2.15 and hepatocytes LO2. HepG2.2.15 cells were divided into ps-miR-122 group (transfected with miR-122 mimic), ps-control group (transfected with mimic control) and control group without treatment. miR-122, NDRG3, hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) expressions were compared in each transfected group. Cell migration, invasion and proliferation were analyzed.Results:Expression of miR-122 in ps-miR-122 group was (2.32±0.05), which was more than that in the control group (0.48±0.09) ( P<0.05). The mRNA and protein expressions of NDRG3 in ps-miR-122 group were (0.45±0.15), (0.43±0.08), which were lower than those in the control group (1.53±0.14), (1.68±0.25) ( P<0.05). The expression levels of HBsAg, HBeAg and HBV-DNA in ps-miR-122 group were (1.05±0.05) IU/ml, (0.69±0.09) NCU/ml and (0.45±0.07) Ig/ml respectively, which were lower than those in the control group (1.51±0.11) IU/ml, (1.32±0.15) NCU/ml and (1.00±0.12) Ig/ml, the differences were statistically significant (all P<0.05). The cell migration rate (33.48±4.12)% and invasion rate (44.11±5.96)% in ps-miR-122 group were lower than those in the control group (91.22±11.45)% and (96.76±12.58)%, and cell proliferation rate at 48 and 72 h were also decreased ( P<0.05). There were no significant differences between ps-control group and control group ( P>0.05). Conclusion:miR-122 may inhibit HBV replication and antigen expression by down regulating NDRG3, and block cell proliferation, invasion and migration of HBV infected hepatocellular carcinoma.

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