Differential Expression of Genes in HepG2 Cells Caused by UC001kfo RNAi as Shown by RNA-seq

The differential expression of genes in HepG2 cells caused by UC001 kfo RNAi was investigated using RNA-seq. HepG2 cells were infected by Lenti-sh UC001 kfo lentivirus particles. The expression of UC001 kfo m RNA in the HepG2-sh UC001 kfo cell line was detected by real-time PCR. RNA-seq technology was used to identify the difference in the expression of genes regulated by lnc RNA UC001 kfo in the HepG2 cell line. Gene ontology and signaling pathway analysis were performed to reveal the biological functions of the genes encoding of significantly different m RNAs. The results showed that m RNAs were differentially expressed between the HepG2-sh UC001 kfo cell line and the HepG2 cell line. The UC001 kfo m RNA was significantly down-regulated in the stable cell line HepG2-sh UC001kfo（P〈0.001）. Additionally, we found 19 signaling pathways or functional classifications encompassing 30 genes that played a role in cancer characteristics, cell adhesion, invasion and migration. The results also showed that the expression of many genes associated with cancer cell invasion and metastasis was decreased with the down-regulation of the lnc RNA UC001 kfo. Lnc RNA UC001 kfo may play a role in regulating cancer cell invasion and metastasis. It was suggested that m RNAs were differentially expressed in the HepG2 cell line after the down-regulation of lnc RNA-UC001 kfo. Some took part in the extracellular matrix, cell adhesion, motility, growth, and localization. The genes encoding of differentially expressed m RNAs may participate in cell invasion and metastasis.

Nuclear matrix associated protein PML: an arsenic trioxide apoptosis therapeutic target protein in HepG2 cells

Objective To investigate arsenic trioxide (As 2O 3)-induced apoptosis and the effects on cell nuclear matrix related protein promyelocytic leukaemia (PML). Methods HepG2 cells were cultured in MEM medium and treated with 0.5, 2, 5 and 10 μmol/L As 2O 3 for either 24 h or 96 h at each concentration. In situ terminal deoxynucleotidyl transferase (TdT) labeling (TUNEL) and DNA ladders were used to detect apoptosis. Confocal microscopy and Western blotting were used to observe the expression of PML. Results The growth rates of HepG2 cells were slower in the As 2O 3 treated than the untreated control group. DNA ladder and TUNEL positive apoptotic cells could be detected in As 2O 3 treated groups. The expression of PML decreased in HepG2 cells with 2 μmol/L As 2O 3 treatment. Confocal images demonstrated that the expression of PML protein in HepG2 cell nuclei decreased after treatment with 2 μmol/L As 2O 3, and micropunctates characteristic of PML protein in HepG2 cell nuclei disappeared after treatment with 5 μmol/L As 2O 3.Conclusions Our results show that arsenic trioxide can significantly inhibit the growth of HepG2 cells in vitro. As 2O 3 induces apoptosis in HepG2 tumor cells in a time and concentration dependent manner. As 2O 3 may degrade the PML protein in HepG2 cell nuclei. The decreased expression of PML in As 2O 3 treated tumor cells is most likely to be caused by apoptosis. Nuclear matrix associated protein PML could be the target of As 2O 3 therapy.

Anti-hepatitis B Virus Activity of 8-epi-Kingiside in Jasminum officinale var. grandiflorum

Objective To evaluate the effect of 8-epi-kingiside (8-Epik) derived from the buds of Jasminum officinale var. grandiflorum (JOG) on hepatitis B virus (HBV) replication in HepG2 2.2.15 cell line in vitro and duck hepatitis B virus (DHBV) replication in ducklings in vivo. Methods The concentration of extracellular hepatitis B e antigen and hepatitis B surface antigen (HBsAg) in cell culture medium was determined by ELISA, respectively. The anti-HBV effects of 8-Epik were also demonstrated in the model of DHBV. 8-Epik was ip given (20, 40, and 80 mg/kg, twice daily) to the DHBV-infected ducklings for 10 d. The isotonic saline liquid diet was ip given as negative control and Lamivudine (50 mg/kg, twice daily) was given as positive control. DHBV DNA was measured at days 0 (T0), 5 (T5), 10 (T10), and day 3 after cessation of treatment (P3) by dot blotting. Results 8-Epik effectively blocked HBsAg secretion in HepG2 2.2.15 cells in a dose-dependent manner [IC 50 = (19.4 ± 1.04) μg/mL]. 8-Epik (40 or 80 mg/kg, ip, twice daily) also reduced viremia in DHBV-infected ducks. Conclusion Therefore, 8-Epik is warranted as a potential therapeutic agent for HBV infection.