Research on the Effects and Mechanisms of Lipoxin-Receptor Agonist BML-111 on H22 Cell Proliferation and Metabolism

This study aims to investigate the effects and mechanisms of lipoxin-receptor agonist BML-111 on H22 cells. Mouse liver cancer cell line H22 was used to construct tumor related in vitro and in vivo models, and lipoxin-receptor agonist BML-111 and lipoxin-receptor blocker BOC-2 were administered as the treatment group and blocker group, respectively. In vivo experiments were conducted to determine the mass and volume of subcutaneous tumors in mice. For in vitro experiments, CCK8 method was used to detect cell viability, kit method was used to detect cell lactate content, glucose content, ATP content, and glutamine metabolism. Western blot was used to detect the protein content of PTEN (phosphatase and tensin homolog deleted on chromosome ten). qRT-PCR method was used to detect PTEN mRNA expression. The mass and volume of subcutaneous tumors in the treatment group decreased compared with the CON group and the blocker group. Compared with the CON group, BML-111 could inhibit the vitality of liver cancer cells, significantly reduce glucose content, lactate content, and glutamine content in H22 cells (P<0.05). Meanwhile, BML-111 could increase the expression level of PTEN, while the lipoxin-receptor blocker BOC-2 could reverse all of these phenomena. BML-111 inhibits the proliferation and energy metabolism of liver cancer cells by reducing glycolysis and glutamine metabolism. Its mechanism of action may be related to the regulation of PTEN expression.

CSTR: 32200.14.cjcb.2025.01.0007