Fig. 4.

Mithramycin A suppresses Fuc-Hp production at the fucosylation level in HepG2 cells.

A) Viability of HepG2 cells treated with increasing doses of mithramycin A. Cell viability was normalized to vehicle control. Data are shown as the average ± S.D. (N = 3 for each condition). B) SLC35C1 expression in HepG2 cells treated with mithramycin A. RPL4 was used as the reference gene, and data are shown as the average ± S.D. (N = 3 for each condition). *p < 0.05. C) The concentration of Fuc-Hp (left) and total Hp (right) in the culture supernatant of HepG2 cells treated with mithramycin A. Data are presented as the average ± S.D. (N = 3 for each condition). *p < 0.05. D) SLC35C1 expression in HepG2 cells stimulated with IL-6 and treated with mithramycin A. RPL4 was used as the reference gene, and data are shown as the average ± S.D. (N = 3 for each condition). E) The concentration of Fuc-Hp (left) and total Hp (right) in the culture supernatant of HepG2 cells stimulated by IL-6 and treated with mithramycin A. Data are presented as the average ± S.D. (N = 3 for each condition). *p < 0.05. F) A schematic illustration describing the SP1-mediated SLC35C1/GFT induction activates the protein fucosylation machinery to upregulate the Fuc-Hp level.