Fig 2: KGM enhances 5-FU-induced ER stress via PERK/ATF4/CHOP signaling. (A) HCC cell ROS levels under different treatments (0.5 µM 5-FU, 6 µg/mL KGM) were measured by flow cytometry. (B–C) Malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in Bel-7402/5-FU and HepG2/5-FU cells under the indicated treatments. (D and E) ATF4 or CHOP mRNA levels in HCC cells resistant to 5-FU or under treatment with PD98058 (20 µM). (F) The protein expression of p-PERK, PERK, ATF4 and CHOP under different treatments in Bel-7402/5-FU and HepG2/5-FU cells. **p < 0.01.

Fig 3: KGM enhances 5-FU-induced ER stress by suppressing TLR4 to activate PERK/ATF4/CHOP signaling. (A) ROS levels in cells under the indicated treatments. (B and C) The effect of TLR4 overexpression on MDA and 8-OHdG levels in KGM and 5-FU cotreated HepG2/5-FU and Bel-7402/5-FU cells was evaluated using an MDA Assay Kit and 8-OHdG ELISA Kit, respectively. (D and E) qRT?PCR was used to measure ATF4 and CHOP mRNA expression in HCC cells with 5-FU resistance in the indicated groups. (F) Western blotting was used to detect the protein expression of p-PERK, PERK, ATF4 and CHOP in Bel-7402/5-FU and HepG2/5-FU cells under different treatments. **p < 0.01.