Skip to main content
. 2022 May 24;6(9):2474–2487. doi: 10.1002/hep4.2014

FIGURE 4.

FIGURE 4

Inhibition of the nonhomologous end joining (NHEJ) pathway enhances the antiviral effect of HBV‐CRISPR in HBV‐infected hepatoma cells. (A–C) HepG2‐hNTCP‐C4‐iCas9 cells transduced with HBV gRNA were treated with DOX 4 days after HBV inoculation (10,000 GEq/cell) and then with siRNA 7 and 10 days after HBV inoculation. (A) Experimental protocol. (B) Expression levels of LIG4, cccDNA, and pgRNA in HBV gRNA–transduced HepG2‐hNTCP‐C4‐iCas9 cells 13 days after HBV inoculation (n = 4; *p < 0.05, **p < 0.01, siLIG4‐treated group vs. siNC‐treated group). (C) Expression levels of BRCA1, BRCA2, cccDNA, and pgRNA in HBV gRNA–transduced HepG2‐hNTCP‐C4‐iCas9 cells 13 days after HBV inoculation (n = 4; *p < 0.05, **p < 0.01, siBRCA1‐treated group or siBRCA2‐treated group vs. siNC‐treated group). BRCA, breast cancer susceptibility gene; LIG4, DNA Ligase 4.