Journal of oral microbiology · 2026
Cell-type-specific actions of carnosic acid against Porphyromonas gingivalis-induced proliferation in liver cancer cells.
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Wang Ting, Chiba Toshimi, Ishikawa Taichi, Kuroda Hidekatsu, Kakisaka Keisuke
Аннотация
BACKGROUND AND AIM: The periodontal pathogen Porphyromonas gingivalis (Pg) has been linked to systemic diseases, including cancer.
OBJECTIVE: To investigate the oncogenic effects of Pg and its lipopolysaccharide (LPS) on liver cancer cells and evaluate the anti‑cancer potential of carnosic acid (CA).
DESIGN: HepG2, HuH7 and pancreatic cancer cells were treated with Pg, Pg‑LPS or CA. Proliferation was assessed by viability assay. Key phosphorylated signaling molecules and their total proteins (TLR4, ERK, Akt, NF‑κB, Nrf2) were examined by western blot and immunofluorescence.
RESULTS: Pg promoted proliferation in HepG2 and pancreatic cancer cells in an MOI‑dependent manner and upregulated TLR4, p‑ERK, p‑Akt and p‑NF‑κB. Pg‑LPS enhanced proliferation, but CA did not inhibit this effect. In HuH7 cells, CA inhibited proliferation, associated with Nrf2 activation; in HepG2 cells, CA showed no inhibition or Nrf2 activation.
CONCLUSIONS: Pg promotes oncogenic processes. CA modulates proliferation in a cell‑type‑ and concentration‑dependent manner, likely through Nrf2 activation.
OBJECTIVE: To investigate the oncogenic effects of Pg and its lipopolysaccharide (LPS) on liver cancer cells and evaluate the anti‑cancer potential of carnosic acid (CA).
DESIGN: HepG2, HuH7 and pancreatic cancer cells were treated with Pg, Pg‑LPS or CA. Proliferation was assessed by viability assay. Key phosphorylated signaling molecules and their total proteins (TLR4, ERK, Akt, NF‑κB, Nrf2) were examined by western blot and immunofluorescence.
RESULTS: Pg promoted proliferation in HepG2 and pancreatic cancer cells in an MOI‑dependent manner and upregulated TLR4, p‑ERK, p‑Akt and p‑NF‑κB. Pg‑LPS enhanced proliferation, but CA did not inhibit this effect. In HuH7 cells, CA inhibited proliferation, associated with Nrf2 activation; in HepG2 cells, CA showed no inhibition or Nrf2 activation.
CONCLUSIONS: Pg promotes oncogenic processes. CA modulates proliferation in a cell‑type‑ and concentration‑dependent manner, likely through Nrf2 activation.