Cell-type-specific actions of carnosic acid against Porphyromonas gingivalis-induced proliferation in liver cancer cells.

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.